The increased expression of PPARA further led to the transcriptional activation of ACSL1, resulting in triglyceride and cholesterol formation in hepatocellular carcinoma (HCC).[148] Moreover, highly‐expressed lncRNA PRADX activated the phosphorylation of STAT3 to promote the expression of ACSL1 by suppressing the expression of BLCAP (a tumor suppressor gene) in mesenchymal glioblastoma (GBM).[149] The upregulated ACSL1 further played roles in basal respiration, proton leak, and ATP production to promote energy metabolism and tumorigenesis of mesenchymal GBM cells. This evidence concerns the gene ACSL1 and hepatocellular carcinoma.