In contrast, dormant tumor cells tend to reduce glucose consumption and shift toward mitochondrial oxidative respiration.163,164 HER2+ breast cancer cells are characterized by CD36 overexpression to facilitate the uptake of exogenous fatty acids, a metabolic preference that confers resistance to HER2-targeted therapies.165 The phenomenon of “glutamine addiction”, a critical metabolic alteration in cancer cells caused by mutations or loss of essential autophagy genes, is also manifested in breast cancer. Here, CD36 is linked to breast carcinoma.