Since the activated PI3K/AKT pathway was reported to cross-talk with stimulated muscarinic receptor signaling33,34, and activated AKT is associated with MYCN expression in contributing to NEPC transformation35, we hypothesized that stimulation of the NGF–CHRM4 axis might upregulate AKT-MYCN signaling in prostate cancer. This evidence concerns the gene AKT1 and prostate cancer.