In inflammatory conditions and cancer, exposure to IFN-γ or to high concentrations of TGF-β1 restrain the immune attack by downregulating HSC activity in bone marrow (15, 16, 34) and by slowing down hematopoietic progenitor cell differentiation in lymph nodes (146), while α-MSH and IGF-1 promote the immune attack by accelerating HSC renewal and proliferation (19, 20). This evidence concerns the gene TGFB1 and cancer.