Interestingly, although it seems that the treatment of cells with Akt inhibitor did not alter palmitate-induced steatosis and ER stress responses, Akt inhibitor partly reversed the effect of CCR2 inhibitor on steatosis and SREBP1c expression, suggesting that the effect of CCR2 blockade, including reduced steatosis and ER stress, might be partially through increased Akt signaling. Here, AKT1 is linked to steatosis.