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. This evidence concerns the gene VCAM1 and acute myeloid leukemia.