The clinical observations that MYCN amplification and/or N-Myc overexpression is found in both NEPC and PCA [5, 28], together with the mechanistic studies showing that N-Myc suppresses AR signaling[13, 22], suggest that 1) MYCN amplification event can arise early in PCA before hormonal therapy; 2) N-Myc overexpression activates other AR-independent pro-survival mechanisms/pathways to allow the cells with N-Myc overexpression to repopulate the tumor after hormonal therapy, and therefore drives the resistance development to AR-targeted therapies. This evidence concerns the gene MYCN and neoplasm.