In this organ, processes such as cellular proliferation, survival, and tumorigenesis were described upon ACh stimulation; in addition, some authors suggested that ACh acted as a mediator via M3 in gastric cancer cell lines, where M3 and M1 receptors were highly expressed [33,108,109] and M3 antagonists decreased cancer growth in mice gastric cells [110], and losing M3 expression in NMU-induced tumors reduced proliferation rate [107]. The gene discussed is CHRM1; the disease is cancer.