For example, there is a known increase in specific pro-inflammatory cytokines (IL-1, IL-6, IL-8, and TNF- α) associated with tobacco use.30,31 These cytokines promote oxidative stress, enhance activation of stellate cells, and subsequently result in liver fibrosis.31 In a higher-risk substrate already predisposed to hepatic steatosis and insulin resistance (such as someone with T2DM), the inflammatory damage tobacco causes may serve as a catalyst for accelerated fibrosis. Here, CXCL8 is linked to Hepatic steatosis.