More importantly, I-PostC significantly reduced the levels of HMGB1, IL-6, and Beclin 1, suggesting that I-PostC could inhibit the HMGB1 expression, inflammatory cascade, autophagy activation, and regulate the interaction between tissue inflammatory response and autophagy in the renal tissue after LIR, preventing kidney damage. The gene discussed is HMGB1; the disease is Nephropathy.