Still, additional experiments are needed to confirm this miR-mediated phenotype, for example, by doing glucose tolerance testing and assessment of whether glucose uptake is indeed due to insulin resistance or due to the observed reduced expression of Glut4. The fact that miR-224 is known to control FA metabolism of 3T3-L1 adipocytes (51), prevents 3T3-L1 apoptosis upon inflammation (52) and controls low-density lipoprotein (LDL) metabolism (via its target PCSK9) (53) is consistent with the notion that miRs coordinately regulate functionally related genes in similar processes (54). This evidence concerns the gene SLC2A4 and Insulin resistance.