Xing et al. [22] found that the CD73-TGFβ dual-blockade may promote a multifaceted inflammatory tumor microenvironment, as shown by the diminished levels of myeloid-derived suppressor cells (MDSCs) and M2-macrophages, and substantially increased levels of activated dendritic cells, cytotoxic T cells, and B cells. Here, TGFB1 is linked to neoplasm.