Studies suggest that M2 TAMs, but not M1 TAMs, enhance tumor hypoxia that promotes angiogenesis by driving transcription of angiogenesis-associated genes, such as VEGF, PDGF, and PGE2 (Squadrito and De Palma, 2011; Jetten et al., 2014); importantly, failure of anti-angiogenic treatments by VEGF inhibitors is caused by the induction of other compensatory pro-angiogenic factors secreted by Tie2-expressing CD11b+ monocytes infiltrating tumor tissues (Belgiovine et al., 2016). The gene discussed is TEK; the disease is neoplasm.