Given the role of immune cell p16INK4a, given the association of the CDKN2A locus to cardiovascular disease and type 2 diabetes and given the effects of bone marrow CDKN2A-deficiency on atherosclerosis development, we investigated the contribution of bone marrow p16INK4a-deficiency to the development of obesity, glucose intolerance and atherosclerosis in appropriate mouse models. This evidence concerns the gene CDKN2A and Glucose intolerance.