Huertas et al. (2012) reported that dysfunctional endothelial cells from idiopathic pulmonary arterial hypertension (IPAH) patients produced increased levels of leptin, and a higher proportion of their Treg expressed leptin receptor. The authors hypothesize that leptin disregulates Treg and contributes to disease (Huertas et al., 2012). In addition, studies in mouse models of atherosclerosis revealed a critical role for leptin in the alteration of the regulatory immune response. Defective LepR signaling improved Treg, function and led to dramatic decreased in lesion size (Taleb et al., 2007). The gene discussed is LEPR; the disease is atherosclerosis.