Consistent with our findings, other experimental strategies (i.e., microRNA 33 (miR-33) antagonism and cholesteryl ester transfer protein (CETP) inhibition) aimed at increasing circulating HDL levels and inducing the m-RCT were also reported to exert long-term, adverse metabolic effects on obese mice [33,34,35], including increased weight gain [35], dyslipidemia [34], and steatosis [33,34]. This evidence concerns the gene CETP and metabolic syndrome.