TGFB1 and acute myeloid leukemia: In contrast, IRF8 also has been shown to promote HL-60 proliferation via the transforming growth factor (TGF)-β receptor/TAK-1/p38 pathway [18], and enhance cell motility and invasion by repressing TGF-β signaling in U2OS cells [19], as well as acting as an independent adverse factor in acute myeloid leukemia [31].