recently demonstrated in mouse models of lung and breast cancer metastasis that Cav-1 inhibition in the so-called metastasis-associated macrophages (MAMs) drives metastatic growth favoring angiogenesis by the restriction of vascular endothelial growth factor A/vascular endothelial growth factor receptor 1 (VEGF-A/VEGFR1) signaling and its downstream effectors at the metastatic site28. Here, FLT1 is linked to breast carcinoma.