In line with this view, previous studies have shown that ACLY and the mitochondrial citrate transporter SLC25A1 contribute to the maintenance of cancer stem cell–like properties: knockdown of ACLY suppresses self-renewal capacity and tumorsphere formation in models of NSCLC, HCC, and breast cancer [50,51], whereas SLC25A1 overexpression in NSCLC and liver cancer stem cells promotes self-renewal, enhances the expression of canonical stemness markers, and is required for proper mitochondrial function [52,53]. The gene discussed is ACLY; the disease is non-small cell lung carcinoma.