They suggested that similar to AMKL myelofibrosis, abnormal blasts in TAM proliferate in the liver during the fetal period, producing excessive cytokines, including TGF-β1, PDGF, and PF4, which stimulate growth and collagen synthesis in fibroblasts to cause liver fibrosis (12). Here, TGFB1 is linked to myelofibrosis.