Several studies have proved that somatic missense mutations in AR are closely associated with important molecular functions of AR, such as transcription activation, protein localization, protein stability, and dimer formation of AR, leading to the growth and survival of prostate cancer cell and causing drug resistance to anti-androgen treatment, ultimately resulting in highly malignant castration-resistant prostate cancer (CRPC)7,8. The gene discussed is AR; the disease is prostate carcinoma.