However, it is important to note that contact-inhibited cells undergo cell cycle arrest, but do not senesce. In fact, it has been shown that contact-inhibited cells resume normal proliferation and mitogen signaling upon being replated in a less confluent culture. Thus, contact inhibition of proliferation may be viewed as a reversible form of cell cycle arrest. Furthermore, to transition from cell cycle arrest to senescence, contact-inhibited cells must activate growth-activating pathways such as mTOR. Once cells in high-density cultures become confluent enough such that the cell area falls below a critical value, the adhesion formations trigger pathways that downregulate mitogen signaling and cell proliferation. The growth-promoting mTOR pathway is therefore inhibited, and consequently the contact-inhibited cells cannot transition from cell cycle arrest to senescence. This has crucial implications in cancer therapy; even though cancer cells are not contact-inhibited, confluent cancer cell cultures still suppress their senescence machinery. Therefore, this may be a plausible explanation why senescence-inducing cancer therapy drugs are ineffective.