Rapamycin has previously been established to inhibit both mitochondrial biogenesis (Cunningham et al., 2007) and oxidative phosphorylation by existing mitochondria (Schieke et al., 2006; Ramanathan and Schreiber, 2009), raising the possibility that a buildup of lipid intermediates due to insufficient fatty acid oxidation might trigger insulin resistance through the PKCθ to IRS1 signaling cascade in rapamycin-treated cells (Morino et al., 2006). Here, PRRT2 is linked to Insulin resistance.