Taken together, our findings support a model wherein ADT or AR inhibitor treatment stimulates ZBTB46 expression, which upregulates NGF-mediated CHRM4 stimulation; this plays a pivotal role in integrating AKT and MYCN signals to promote therapeutic resistance and neuroendocrine differentiation of prostate cancer (Fig. 7h). This evidence concerns the gene AKT1 and prostate carcinoma.