 the price to 0 and heres why.

Let’s say I was a hedge fund starting to seeing huge losses because of that June squeeze. Well I’m deep under water and I gotta make all that money back plus a billion more because I’m a greedy fuck. So what I do is let the price sky rocket, just under where I entered my short position (based on the average short holding period from ortex that price is around the $50 mark and if you look at that charts, that’s exactly where we’ve been getting knocked down recently) sell calls on the way up and add onto my short position or buy puts on the way down. They do this as much as they want it’s already happened towards the end of July. Bam money printing machine and we didn’t have the slightest idea.

There’s another reason why they’re not getting out of their short position. Let’s be honest AMC is not going to stay at insane highs forever. And you know what’s an insane way of making profits, shorting a stock at $500 and waiting for it to come back to $1. They’re doing the same thing we’re doing holding and adding their shorts their mentality is the same hodl short on the way down. 

The only way this blows up is if A) stock price gets out of control, they get margins called at insane levels and gg. B) Government agencies step in to regulate the markets more or C) they have no incentive to keep driving the price up and down in the same levels which again comes from us just giving them premiums for their options contracts just for them to expire worthless.Chris Anderson wrote an article that became a book on a phenomenon about business called the Long Tail. There is a lot of business in the Long Tail. Niche Marketing. It's how blogs work: there are tens of millions of blogs with anywhere from millions of readers to none. It is a carry-over from Pareto Principle of 80/20, where 80% of your revenue comes from 20% of your clients. "But where the Long Tail works, minority tastes are catered to, and individuals are offered greater choice." Tom Peters says that marketing to Women is the single business idea that can advance sales (if done right). The Hispanic market is huge. The Retiree market is huge - just look at all the active lifestyles communities built in FL and Calif. Where is this going? You can't be everything to everybody - that's what cable and telcos do because they have huge ad budgets. You need to find out what your Niche is and sell deep to that segment for greater success.Cancer Cell. 2014 Feb 10;25(2):139-51. doi: 10.1016/j.ccr.2014.01.008.
Justilien V1, Walsh MP1, Ali SA1, Thompson EA1, Murray NR1, Fields AP2.
Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA.
Department of Cancer Biology, Mayo Clinic Cancer Center, Jacksonville, FL 32224, USA. Electronic address |||EMAIL_ADDRESS||| We report that two oncogenes coamplified on chromosome 3q26, PRKCI and SOX2, cooperate to drive a stem-like phenotype in lung squamous cell carcinoma (LSCC). Protein kinase Cι (PKCι) phosphorylates SOX2, a master transcriptional regulator of stemness, and recruits it to the promoter of Hedgehog (Hh) acyltransferase (HHAT) that catalyzes the rate-limiting step in Hh ligand production. PKCι-mediated SOX2 phosphorylation is required for HHAT promoter occupancy, HHAT expression, and maintenance of a stem-like phenotype. Primary LSCC tumors coordinately overexpress PKCι, SOX2, and HHAT and require PKCι-SOX2-HHAT signaling to maintain a stem-like phenotype. Thus, PKCι and SOX2 are genetically, biochemically, and functionally linked in LSCC, and together they drive tumorigenesis by establishing a cell-autonomous Hh signaling axis.
A) Phase contrast photomicrographs of H1703, ChagoK1 and H1299 parental adherent cells (top panels), oncospheres in low adherence culture (middle panels) and redifferentiated oncosphere cells after return to adherent culture (bottom panels). B) QPCR for putative stem cell markers expressed as fold of parental cells +/−SEM, n = 3; *p<0.05 versus NT adherent cells. Results are representative of five independent experiments. C) Photomicrographs showing clonal expansion of individual cells into oncospheres over a 15 day period. D) Anchorage-independent growth expressed as mean fold-change from parental cells +/− SEM. n = 5, * p<0.05 versus NT adherent cells. Results are representative of five independent experiments. E) Formation of lung orthotopic tumors in immunocompromised mice. 10,000 parental H1299 adherent or oncosphere cells were implanted into the lungs of immune-deficient mice. Lateral and dorsal views of bioluminescent images of a tumor-bearing mouse (a) and corresponding bioluminescence image upon lung dissection (b). H&E of typical parental and oncosphere tumors (c). Oncospheres develop primary tumors at the site of injection (arrows) and multiple lesions to the ipsilateral and contralateral lobes of the lung (arrowheads); parental cells develop either a single, small tumor at the site of injection (shown) or no identifiable tumor. 40X magnification reveals the similar morphology of oncosphere- and parental cell-derived tumors (d). Incidence of tumor formation in limiting dilutions of H1299 oncosphere and parental cells (e). Quantification of tumor growth by IVIS (f); Mean +/−SEM. *p<0.05 n=5, *p<0.05 vs. parental cells. See also.
Cancer Cell. ;25(2):139-151.
A) Effect of RNAi-mediated PKCι knockdown (immunoblot) on anchorage-independent growth of H1703, H1299 and ChagoK1 oncospheres. Results are expressed relative to NT RNAi control cells +/− SEM, n = 5; **p<0.001. B) Oncosphere size expressed as mean diameter in μm +/−SEM. n=98 (H1703), 138 (H1299) and 44 (ChagoK1). C) QPCR for HHAT, GLI1, ADRBK1 and CDK19. Results are expressed as fold NT parental cells +/−SEM, n=3; *p<0.05 compared to NT parental. Results are representative of three independent experiments. D) Effect of SMO inhibitor LDE225 on H1703, H1299 and ChagoK1 oncosphere (onco.) and parental cell (par.) proliferation. Results expressed as % DMSO control +/−SEM; n=6. Results are representative of three independent experiments. See also and, and.
A and B) RNAi-mediated knockdown of HHAT and GLI1 in H1299 oncospheres, respectively, expressed as fold of NT RNAi control +/− SEM n=3. *p<0.0005 compared to NT control. C) Effect of HHAT or GLI1 RNAi on clonal expansion expressed as oncosphere diameter in μm +/− SEM, n>15 per RNAi sample; *p<1.0×10−06. Data are representative of three independent experiments. D) Soft agar growth expressed relative to NT RNAi control cells +/− SEM, n = 5; * p<0.003. Data are representative of three independent experiments. E) NT, PKCι, HHAT and GLI1 oncospheres were treated with the indicated amounts of Hh-Ag1.5, a selective Hh agonist, and cell proliferation assessed by MTT at 5 days. Results expressed as % of NT DMSO control +/− SEM, n = 6. F) Detection of palmitoylated SHH in oncospheres. Parental (P) and oncosphere (O) NT, PKCι and HHAT RNAi cultures expressing FLAG-SHH were metabolically labeled with w-alkynyl-palmitate (C16) and palmitoylated SHH (palm-SHH) and total SHH were detected as described in Experimental Procedures. G) Oncosphere growth as lung orthotopic tumors. NT parental and NT, PKCι, HHAT, and GLI1 RNAi oncosphere tumor growth was monitored by bioluminescence detected by IVIS imaging. Data are presented as total flux in photons per second ± SEM; n = 10 per group except for PKCι where n=9; *p<0.05 significantly different than NT RNAi oncosphere tumors. See also.
A) RNAi-mediated knockdown of SOX2 in H1299 oncospheres. Results expressed as % NT control +/−SEM; n=3, *p<0.05. B) Clonal expansion expressed as oncosphere diameter in μm +/− SEM; n> 22 per RNAi sample, p< 3.0 ×10−14 and are representative of three independent experiments. C) Anchorage-independent growth relative to NT RNAi control cells +/− SEM, n = 5; *p<5.0×10−9. Results are representative of three independent experiments. D) Chromatin immunoprecipitation (ChIP) analysis to assess SOX2 occupancy of the HHAT promoter. Schematic depicts the HHAT promoter region; the position of ChIP probes used are indicated (A and B); Consensus SOX2 binding sites are indicated by vertical slashes. Data presented as % of input; n=3