Several lines of evidence support this hypothesis, as the expression of p16INK4a in H‐NSCs was much higher in VD rats, the intensity of SA‐β‐gal and the expression of p16INK4a, γ ‐H2AX, P21, P53 in isolated H‐NSCs neurospheres were increased in a time‐related manner. The gene discussed is TP53; the disease is sexually transmitted disease.