Since the progression of liver cancer depends on oxidative phosphorylation and fatty acid metabolism to facilitate the self-renewal and tumor-initiation abilities of LCSCs, Activation of the LPL/FABP4/CPT1 axis in NASH may represent a metabolic reprogramming that promotes tumorigenesis by nurturing oncogenic signal-driven TICs, thus promoting the development of NASH to HCC. The gene discussed is LPL; the disease is metabolic dysfunction-associated steatohepatitis.