This is interesting in light of recent evidence demonstrating that macrophages and HSCs are susceptible to lipotoxic damage characterized by excessive fat storage and oxidative stress, and causally contribute to NASH initiation and progression by stimulating inflammation and fibrogenesis.40,50 Notably, in this study, we did not find any evidence that the silencing of TAOK1 would reduce lipid storage or oxidative stress in liver nonparenchymal cells. The gene discussed is TAOK1; the disease is metabolic dysfunction-associated steatohepatitis.