In separate studies, treatment with an HDAC1 inhibitor (i.e., MS-275) (Ferrari et al., 2017a; Rajan et al., 2018) and genetic ablation of HDAC9 (Chatterjee et al., 2014a,b) and HDAC11 (Bagchi et al., 2018) in HFD-fed mice alleviate the obesity phenotype as a result of reduced body weight (Chatterjee et al., 2014a,b; Ferrari et al., 2017a; Rajan et al., 2018), improved glucose tolerance (Ferrari et al., 2017a; Rajan et al., 2018), and increased thermogenesis and “browning” of WAT (Chatterjee et al., 2014a,b; Ferrari et al., 2017a; Rajan et al., 2018). The gene discussed is HDAC9; the disease is obesity due to melanocortin 4 receptor deficiency.