The lncRNA FTX was downregulated and the lncRNA SNHG20 was upregulated in NAFLD-related HCC tumor tissues, and FTX supplement and SNHG20 silencing inhibited the conversion of NAFLD to HCC, which prompted out interest in explorng its potential as a future HCC risk predictor [56,57]. This evidence concerns the gene FTX and metabolic dysfunction-associated steatotic liver disease.