Nonetheless, it is important to acknowledge that angiogenesis in ALL involves a complex interplay of additional pro‐angiogenic factors, including bFGF, PDGF, and hypoxia‐inducible factor‐1α (HIF‐1α), which act synergistically within the bone marrow microenvironment to promote leukemic cell expansion, vascular remodeling, and resistance to treatment [56]. The gene discussed is FGF2; the disease is acute lymphoblastic leukemia.