SELE and acute myeloid leukemia: In an AML murine model bearing the human KMT2A-MLLT3 oncogene, the small molecule E-selectin mimetic GMI-1271/Uproleselan has enhanced the efficacy of AML treatment by overcoming vascular niche-mediated chemoresistance, indicating E-selectin blockade alleviates pro-survival signaling and improving therapeutic efficacy (150).