In patients with obesity, adipose tissue-associated and circulating T cells are preferentially skewed towards inflammatory Th1- and/or Th17-type T cells and studies have shown that IFN-γ and IL-17A contribute to aberrant glucose and lipid homeostasis in several cell types, including adipocytes [38–40, 76]. The gene discussed is IFNG; the disease is obesity due to melanocortin 4 receptor deficiency.