It could be postulated that the mechanisms of anti-angiogenic action are attributable to (i) the inability of PlGF to bind to the receptor, which would, in turn, hamper (ii) the suppression of the migration of myeloid progenitor cells into the tumor microenvironment and the infiltration of the TME by M2 macrophages, as well as (iii) the reduction in VEGFR-1 expressing cancer cell survival. This evidence concerns the gene FLT1 and neoplasm.