Altogether, these findings underscore the importance of genetic variants in DDR genes—particularly those involved in homologous recombination (XRCC2 and RAD51C), checkpoint control (ATM, CHEK1, and TP53), and excision repair pathways (ERCC1 and ERCC2)—in modulating individual susceptibility to both acute and late radiation-induced skin toxicity. The gene discussed is RAD51C; the disease is dermatological toxicity.