CDKN2A and Hepatic fibrosis: This transgenic mouse model under the control of a 2.6 kB p16INK4A-promoter fragment might not completely reflect endogenous p16INK4A expression and regulation as we detected p16INK4A expression in the heart and liver [38,39] and elimination of p16INK4A expressing cells in the p16INK4ACre;DTA model caused cardiac and liver fibrosis and reduced health span [39], which is in agreement with the notion that senescent cells contribute to tissue repair and maintenance [211,221].