The decrease in AchE activity leads to elevate Ach levels in NSCLC cells, which could promote cell proliferation, migration, invasion, angiogenesis, and reduce apoptosis/autophagy through activating Ca2+ channels, TGF-β-induced EMT and α7nAChR-mediated signaling pathways such as PI3K/Akt, ERK/MAPK, GSK-3β, and STAT3 [97]. This evidence concerns the gene TGFB1 and non-small cell lung carcinoma.