After remission of ERS, on the one hand, the expression levels of SREBP-1c and FOXO-1 protein were down-regulated for alleviating FFA-induced steatosis; On the other hand, silencing PKC-δ inhibited the production of inflammatory factors (IL-1β and TNF-α) and ROS and up-regulated the expression of PI3K-p85 and p-AKT protein in order to restoring the transduction pathway of insulin, thus alleviating IR and glucose intolerance in FFA-induced L02 hepatocytes (Fig. 7). The gene discussed is PRKCD; the disease is amelogenesis imperfecta type 1G.