CDK5 has known antiapoptotic roles in thyroid and prostate cancer cells and is known to facilitate the DNA damage repair response, and although CDK5 kinase activity in non-neuronal cells is generally described as p35-dependent, it is possible that other, less studied or unknown coactivators enable CDK5 to continue serving these roles even when p35 expression is ablated (39). This evidence concerns the gene CDK5R1 and prostate cancer.