To test the idea that SnCs might play a causative role in OA, we used the p16-3MR transgenic mouse, which harbors a p16<sup>INK4a</sup> (Cdkn2a) promoter driving the expression of a fusion protein containing synthetic Renilla luciferase and monomeric red fluorescent protein domains, as well as a truncated form of herpes simplex virus 1 thymidine kinase (HSV-TK).