Since we previously observed that p16INK4-deficiency modulates the inflammatory phenotype of murine macrophages [15] and since p16INK4a knock-down directs human macrophages toward an ATM-like phenotype [20], we analyzed the contribution of the bone marrow p16INK4a-deficiency to diet-induced adipose tissue development and glucose intolerance in mice. This evidence concerns the gene ATM and Glucose intolerance.