In support of its radiosensitizing potential in PCa, more recently, El Bezawy et al. demonstrated that miR-145 ectopic expression, resulting in direct inhibition of SPOP, the most commonly mutated gene in PCa, was able to enhance radiation response of PCa both in vitro and in vivo by downregulating RAD51 and CHK1, key players in the HR DDR pathway [97]. This evidence concerns the gene CHEK1 and posterior cortical atrophy.