This is relevant because the overactivation of the PI3k/Akt pathway is a frequent event in human cancers [103,104]; therefore, we could hypothesize that the hyperactivation of PI3k/Akt could decrease AChE content; this event affects the apoptosome formation and enzymatic activity, allowing high ACh levels that promote cell proliferation and inhibition of apoptosis through ACh receptors (AChRs) (Figure 10). This evidence concerns the gene AKT1 and cancer.