Hypoxia promotes the expression of immunosuppressive molecules such as vascular endothelial growth factor (VEGF), TGF-β, IL-10, and PD-L1 and induces the recruitment of cancer-associated fibroblasts (CAF) to facilitate the infiltration of myeloid-derived suppressor cells (MDSCs), Tregs, and type 2 tumor-associated macrophages (TAMs) via hypoxia-induced metabolic alterations in the tumor and TME [254, 255]. This evidence concerns the gene TGFB1 and neoplasm.