Cells overexpressing SULF2 create a microenvironment enriched in specific growth factors (e.g., VEGF, FGF2, Wnt) [40, 41], which strongly promote macrophage polarization, inducing monocyte differentiation into M1/M2-type tumor-associated macrophages (TAMs), and Macrophages co-expressing both M1 and M2 phenotypes, all these components represent potential factors influencing the development of cardiovascular diseases [42]. This evidence concerns the gene FGF2 and neoplasm.