Once activated during NAFLD progression, KCs produce proinflammatory factors, such as monocyte chemoattractant protein 1 (MCP‐1) and tumor necrosis factor (TNF), leading to increased hepatic monocyte recruitment and inhibition of canonical insulin signaling, further aggravating liver injury and steatosis (Aparicio‐Vergara et al, 2013; Wandrer et al, 2020). The gene discussed is CCL2; the disease is steatosis.