Further analysis via CFC assay revealed that self-renewal capacity of HEL cells remained unchanged after treatment with anti-HHLA2 monoclonal antibodies (mAbs) or HHLA2-human Fc fusion protein (Fig. 2i), indicating that TMIGD2-mediated AML function is HHLA2 independent. Here, HHLA2 is linked to acute myeloid leukemia.