However, PPARγ agonists (e.g., thiazolidinediones) cause PPARγ protein to dissociate from the GLUT4 gene promoter and improve insulin resistance, by blocking suppression of GLUT4 mediated by fatty acids (i.e., arachidonic acid) and/or TLR4 agonists (i.e., LPS) and inducing GLUT4 expression via PPARγ activation [53-55]. This evidence concerns the gene SLC2A4 and Insulin resistance.