Collectively, these results indicate that, although the parental CD18/HPAF cancer cells lack a functional G1 checkpoint and thus instead respond to IR with the induction of a G2/M cell cycle arrest, the knockdown of PR55α by shRNA was sufficient to induce high levels of p16 expression, which may have then allowed the bulk of the cells to remain in G1 after IR. The gene discussed is ITGB2; the disease is cancer.