These results demonstrated that (1) increased plasma resistin is derived from increased expression of resistin in white adipose tissues; (2) resistin expression is suppressed by miR-155, thus resistin expression is increased in miR-155 DKO white adipose tissues; and (3) since resistin is a proinflammatory adipokine, high-fat diet induction of resistin upregulation in white adipose tissues makes resistin a potential significant mediator to drive “a second wave of inflammation” in the miR-155-/- MHO status, which is required to MHO transition to classical obesity. The gene discussed is RETN; the disease is obesity due to melanocortin 4 receptor deficiency.