Prior studies have demonstrated that KRAS‐driven lung tumors exhibit increased glucose flux into the tricarboxylic acid (TCA) cycle, with mitochondrial pyruvate metabolism being essential for tumor formation in vivo.[35] In our study, we show that KRAS drives COA4 expression via the PI3K pathway, and that COA4 is markedly overexpressed in LUAD tissues with KRAS mutations or high KRAS expression. Here, KRAS is linked to neoplasm.