In line with a previous report revealing TCA cycle-independent metabolism of glucose-derived citrate in [U-13C] glucose-labeled 82 non-small cell lung cancer lines (Chen et al. 2019), treatment of both human SCLC and mouse embryonic stem (ES) cells with an ACLY inhibitor or knockout of ACLY expression increased mitochondrial malate production, whereas knockout of mitochondrial aconitase (ACO2) reduced mitochondrial malate production (Arnold et al. 2022). This evidence concerns the gene ACLY and small cell lung carcinoma.