TBCE and Hepatic steatosis: PRR signaling in KCs and infiltrating macrophages causes complexing of NOX2 with other proteins (p67, P40, Rac GTPases) to generate superoxide, drive proinflammatory cytokine production (e.g., IL-6, TNF, IL-1β, transforming growth factor-β [TGFβ]) and promote hepatic steatosis, hepatocellular damage and fibrosis (43, 77, 78).