In this study, excessive PKC significantly promoted the expression of the pro-inflammatory factor (il-1β) and inhibited the expression of the anti-inflammatory factor (tgf-β1), These results may be attributed to the continued intestinal accumulation of anti-nutritional factors present in PKC, which compressed and destroyed the integrity of the intestinal epithelial mucosa, and induced enteritis (66, 67). The gene discussed is PRRT2; the disease is enteritis.