Because we did not observe significant changes in the level of CD36 and FABPpm following the administration of 2.5 μM and 5 μM CBG, we hypothesize that the lipid overload conditions led to the permanent upregulation of membrane level of this transporter, which is an early and rapid process, thereby promoting the accumulation of FAs within the FFA, TAG, and PL pools at the onset of insulin resistance, as it was indicated in different obesity studies [36,69,70,71]. The gene discussed is CD36; the disease is Insulin resistance.