Our MHO model has increased plasma resistin compared with ApoE-/- mice as well as increased white adipose tissue-derived resistin, showing that HF feeding can bypass miR-155 deficiency-defined lower inflammation status and accelerate the transition from less inflamed MHO to highly inflamed classical obesity with our newly defined “secondary wave of inflammation status (SWIS).” These experimental data strongly consolidate our new working model on the two types of MHO proposed based on our experimental data analysis. The gene discussed is RETN; the disease is obesity due to melanocortin 4 receptor deficiency.