PDHK4 has also been implicated in an increase in mitochondrial fatty acid β-oxidation through inactivation of acetyl-CoA carboxylase (ACC) by AMP-activated protein kinase phosphorylation.29 Moreover, mutant KRAS expressing tumours also rely on fatty acid metabolism to maintain TCA cycle activity, proliferation and survival.30, 31 To further explore the metabolic effects of PDHK4 and KRAS knockdown on lipid metabolism, we analysed ACC and FASN by western blot in the isogenic cells (Figure 5c). Here, ACACA is linked to neoplasm.