The expression of constitutively active form of Rac1 (Rac1-V12) in HSPCs, promoted the retention of HSCs in the niche having higher CD44, VCAM-1, c-MPL, CXCR4, and N-cadherin, enhancing colony formation, quiescence and preventing leukemia cells from apoptosis [52] suggesting that inhibition of Rac GTPase activity could be an effective way of counteracting AML leukemias. The gene discussed is RAC1; the disease is acute myeloid leukemia.