GATA2 genetic variation reduces HSPC activity and mobilization efficiency. Before treatment, WT quiescent HSPCs are maintained in BM through retention mechanisms including CXCR4/CXCL12, VLA-4/VCAM1, and low inflammation (IL-8). During mobilization, these mechanisms are disrupted, leading to HSPC expansion and circulation. Gata2 variation decreases HSPC levels, reducing the available HSPCs to mobilize and compromises VLA-4/VCAM1- and IL-8–induced mobilization mechanisms.