High expression levels of miR-195 and miR-16 were inversely correlated with PD-L1/PD-1 and CD80/CTLA-4 expression, and the blocking of the PD-L1 immune checkpoint could enhance radiotherapy via activation of the T cell response at the tumor microenvironment in prostate cancer, revealing biological and functional interactions between immunotherapy and radiotherapy through the miR-195/-16 family regulatory cascade [102]. This evidence concerns the gene CTLA4 and Familial prostate cancer.