Similar metabolic plasticity has been documented in breast cancer models, where basal-like breast CSCs frequently exhibit a heightened glycolytic phenotype, as evidenced by elevated expression of enzymes such as hexokinase 2 and lactate dehydrogenase A. In contrast, luminal-subtype CSCs often rely more on OXPHOS, a preference linked to increased mitochondrial biogenesis and respiratory capacity.281 These distinctions reinforce the concept that even within a single tumor type, CSC populations can adopt heterogeneous metabolic strategies to meet their energy and biosynthetic requirements. The gene discussed is LDHA; the disease is breast cancer.