Data on possible communication between EGFR and the cholinergic ligand indicated that overexpression of AChE was detected in HCC cells blocking the activation of MAPK and PI3K/AKT signaling pathway by decreasing the phosphorylation of ERK and AKT; this overexpression also produced an enhancement of the pharmacological effect of drug-induced apoptosis [168]. The gene discussed is ACHE; the disease is hepatocellular carcinoma.