Using different human colon cancer cell lines that express M3R, Cheng et al. and Ukegawa et al. reported that the interactions of both ACh and secondary bile acids with M3R resulted in transactivation of EGFR and downstream phosphorylation of key mediators, including ERK1/2, Akt, and p38 MAPK [146,147,148], provoking cell proliferation and survival. Here, EGFR is linked to colonic neoplasm.