CD109 suppresses TGF-β signaling in HSCs, and the lack of CD109 may increase their sensitivity to TGF-β, thus leading to preferential commitment of erythroid progenitor cells to mature red blood cells in immune-mediated bone marrow failure (74), suggesting that CD109 by modulating TGF-β signaling, regulates this inflammatory response in the bone marrow. Here, CD109 is linked to Bone marrow hypocellularity.