MiR-1307 is overexpressed in prostate cancer cells and tissues, apparently fostering cell propagation and tumorigenesis when a cell cycle blockade is relieved by miR-1307 inhibition of the cell cycle suppressors p21 and p27 at both the mRNA and protein levels, and miR-1307 prevents the biological effects mediated via FOXO3a by directly binding to the 3’-UTR of FOXO3a and promoting cell proliferation in prostate cancer (63). This evidence concerns the gene CDKN1B and prostate cancer.