They demonstrated that ACh could act through CHRM3 to activate the EGFR pathway, while CHRM3 knockdown or EGFR inhibition could reverse the cell proliferation and phosphorylation of ERK and AKT induced by ACh stimulation in gastric cancer by activating non-canonical signals [72] (non-canonical signals include Ras–Raf-1–Erk–AKT for the CHRM3 receptor subtype [83,84]. The gene discussed is AKT1; the disease is gastric cancer.