In vivo mouse tumor models, oxidative metabolism was activated in hypoxic TAMs coupled with glucose intake decreasing, in the meantime, oxidative damage culminating in endothelial cell leading to angiogenesis and metastasis through the upregulation of DNA damage inducible transcript 4 (DDT4, also known as REDD1), an endogenous inhibitor of mechanistic target of rapamycin (MTOR) complex 1 (MTORC1) (78). The gene discussed is DDIT4; the disease is neoplasm.