This switch leads to a phenotype shift from luminal epithelial-like prostate adenocarcinoma to AR-independent, basal-like cells expressing neuroendocrine markers, such as synaptophysin and chromogranin A. RB1 inactivation is the major driver of this lineage crossover to neuroendocrine-type prostate cancer (NEPC). The gene discussed is AR; the disease is Familial prostate cancer.