Several experiments provided evidence that the inhibitory effects of M1R agonism on cell proliferation were not mediated by test agent toxicity or the induction of cellular senescence or apoptosis; after applying test agents (carbachol and McN-A-343) to colon cancer cells, we detected no meaningful changes in LDH release, senescence-activated β-galactosidase activity, or cleaved caspase-3 generation. Here, CHRM1 is linked to colonic neoplasm.