Note: These lists are illustrative, not exhaustive, and identification of noise effects is an active and expanding area of research.
* Gene expression levels: noise in gene expression causes differences in the fundamental properties of cells, limits their ability to biochemically control cellular dynamics, and directly or indirectly induce many of the specific effects below;
* Energy levels and transcription rate: noise in transcription rate, arising from sources including transcriptional bursting, is a significant source of noise in expression levels of genes. Extrinsic noise in mitochondrial content has been suggested to propagate to differences in the ATP concentrations and transcription rates (with functional relationships implied between these three quantities) in cells, affecting cells' energetic competence and ability to express genes;
* Phenotype selection: bacterial populations exploit extrinsic noise to choose a population subset to enter a quiescent state. In a bacterial infection, for example, this subset will not propagate quickly but will be more robust when the population is threatened by antibiotic treatment: the rapidly replicating, infectious bacteria will be killed more quickly than the quiescent subset, which may be capable of restarting the infection. This phenomenon is why courses of antibiotics should be finished even when symptoms seem to have disappeared;
* Development and stem cell differentiation: developmental noise in biochemical processes which need to be tightly controlled (for example, patterning of gene expression levels that develop into different body parts) during organismal development can have dramatic consequences, necessitating the evolution of robust cellular machinery. Stem cells differentiate into different cell types depending on the expression levels of various characteristic genes: noise in gene expression can clearly perturb and influence this process, and noise in transcription rate can affect the structure of the dynamic landscape that differentiation occurs on. There are review articles summarizing these effects from bacteria to mammalian cells;
* Drug resistance: Noise improves short-term survival and long-term evolution of drug resistance at high levels of drug treatment. Noise has the opposite effect at low levels of drug treatment;
* Cancer treatments: recent work has found extrinsic differences, linked to gene expression levels, in the response of cancer cells to anti-cancer treatments, potentially linking the phenomenon of fractional killing (whereby each treatment kills some but not all of a tumour) to noise in gene expression.  Because individual cells could repeatedly and stochastically perform transitions between states associated with differences in responsiveness to a therapeutic modality (chemotherapy, targeted agent, radiation, etc.), therapy might need to be administered frequently (to ensure cells are treated soon after entering a therapy-responsive state, before they can rejoin the therapy-resistant subpopulation and proliferate) and over long times (to treat even those cells emerging late from the final residue of the therapy-resistant subpopulation).
* Evolution of genome: Genome are covered by chromatin that can be roughly classified into "open" (also known as euchromatin) or "closed" (also known as heterochromatin). Open chromatin leads to less noise in transcription compared to heterochromatin. Often "housekeeping" proteins (which are proteins that carry out tasks in the required for cellular survival) work large multiprotein complexes. If the noise in proteins of such complexes are to discoordinated, it can lead to reduced level of production of multiprotein complexes, with potentially deleterious effects.  Reduction in noise may provide an evolutionary selection  movement of essential genes into open chromatin.
* Information processing: as cellular regulation is performed with components that are themselves subject to noise, the ability of cells to process information and perform control is fundamentally limited by intrinsic noise