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). This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.