CXCL12 and acute myeloid leukemia: This outcome is consistent with the finding obtained with the MLL-AF9 murine AML model, where interactions with E-selectin enhanced chemoresistance mediated via AKT/NF-kB pathways.190 In addition to the perisinusoidal niche, Agarwal et al. showed that selective deletion of CXCL12 from periarteriolar Tie2+ MSPCs impaired the proliferation of leukemia stem cells, while CXCL12 expressed in Prx1+ MSPCs reinforce cell quiescence and chemoresistance191 (Fig. 5.9).