RB1 and neoplasm: A small population of M-MDSCs was initially postulated to be able to differentiate into G-MDSCs through downregulation of the retinoblastoma 1 (Rb1) gene [29]; however, this precursor population was later identified as monocyte-like precursors of granulocytes (MLPGs), and MLPGs contributed to up to 50% of the total G-MDSCs in some mouse tumor models [30].