In the CRC microenvironment, TAMs predominantly adopt an M2-like phenotype [135], fostering malignancy through multifaceted mechanisms: secretion of matrix metalloproteinases (MMPs) and growth factors (e.g., VEGF), suppression of M1 macrophage antitumor activity, inhibition of T cell function via PD-L1 expression and arginine metabolism, and synergistic interactions with immunosuppressive cells (e.g., MDSCs, Tregs) [136]. This evidence concerns the gene VEGFA and colorectal carcinoma.