Fibrosis could represent a possible condition allowing TAMs to inhibit T-cell accumulation within the tumor mass: through interaction with fibroblasts, macrophages are known to actively participate in tissue re-modeling, inducing collagen synthesis and secretion [70]; furthermore, by producing granulin, M2-TAMs were shown to remodel the ECM [71] and induce fibrosis in the tumor stroma [72,73]. This evidence concerns the gene GRN and neoplasm.