HMGB1 and Hepatic fibrosis: As a fundamental regulator of signal transduction in protein synthesis, AKT can be transformed into a phosphorylation state via stimulation by activated PI3K [112], which then promotes the release of the inflammatory cytokines TNF-α, IL-1β, and IL-18, thereby stimulating the inflammatory cascade response resulting in damage to various organs and tissues [101].Therefore, HMGB1 seems to play a pivotal role in liver fibrosis by activating HSCs mainly through RAGE receptors to initiate collagen synthesis and deposition in liver fibrosis.