The extent of altered M1-like TAM polarization observed with GM-CSF treatment in the orthotopic model (Fig. 6c) was equivalent to that observed in mice transplanted with shSnail1-depleted 4T1 cells (Fig. 3b), indicating that GM-CSF was likely a major regulator of M1-like polarization in breast tumors lacking SNAIL1. This evidence concerns the gene SNAI1 and breast neoplasm.