The ability of CGK012 to prevent the progression of HMGB1-induced sepsis was examined by investigating its effects on HMGB1 secretion (Figure 2A,B); the expression of HMGB1 signal receptors, such as TLR2, TLR4, and RAGE (Figure 2C); and the HMGB1-induced increase in permeability (Figure 4A–C) by blocking the p38 biochemical modification (Figure 4D) and its pathway. The gene discussed is TLR4; the disease is Sepsis.