Instead, the bone marrow tumour microenvironment, which is rich in TGF-β, converts CD4+ T cells into TH17 cells to blunt anti-CTLA-4 immunotherapy at this site.150 Combining TGF-β inhibitors with anti-CTLA-4 to generate TH1 CD4+ T cell and CD8+ T-cell responses can reverse these effects in metastatic lesions. Here, TGFB1 is linked to neoplasm.