In contrast, in the MASH‐like model, circSMEK1 knockdown led to a significant increase in lipid accumulation (Figure 1R) and enhanced the expression of the pro‐inflammatory and pro‐fibrotic markers TNF‐α and TGF‐β (Figure 1T). These results indicate that circSMEK1 plays a specific and critical role in the progression from steatosis to inflammatory steatohepatitis (MASH), rather than in the initial lipid accumulation stage (MASLD). The gene discussed is TGFB1; the disease is steatosis.