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. The gene discussed is STAT3; the disease is glioblastoma.