Yasumizu et al. demonstrated that the upregulation of the oncogenic C-terminal subunit of MUC1, namely MUC1-C, in AR-dependent prostate cancer cells drives NEPC progression by repressing AR signaling, suppressing the p53 pathway, and inducing N-Myc and EZH2 expression [43]. The gene discussed is TP53; the disease is prostate carcinoma.