Our results demonstrate that the accumulation of ATM in HFD mice, which is a largely described hallmark of obesity and diabetes (Lumeng et al., 2007, 2008; Weisberg et al., 2003; Cani et al., 2007; Fujisaka et al., 2009) originates at least in part from resident AT-LSK and occurs very early in the disease development and is mainly due to enhanced progenitor proliferation. This evidence concerns the gene ATM and obesity due to melanocortin 4 receptor deficiency.