This finding is in-line with an intriguing paradigm of ’parasitic’ tumor-stromal metabolism called the Reverse Warburg Effect (RWE) [33] which suggests that tumor cells ’hijack’ CAFs by inducing oxidative stress and downregulating stromal Cav-1 to promote catabolic processes that supply nutrients to tumor cells for anabolic growth and survival thereby promoting tumor progression, metastasis, and resistance to therapy. Here, CAV1 is linked to neoplasm.