The authors identified that Cav-1-deficient stromal fibroblastic cells show a markedly reduced mitochondrial reserve capacity and a mitochondrial defect in Cav-1-deficient stromal cells which may drive oxidative stress, leading to aerobic glycolysis (HIF-1α) and inflammation (NFκB) in the tumor microenvironment. The gene discussed is CAV1; the disease is neoplasm.