HHLA2 and acute myeloid leukemia: By taking the advantage that both of our anti-TMIGD2 mAb 17C7 and anti-HHLA2 mAb B5B5 can completely block the interaction between HHLA2 and TMIGD2, we treated AML PDX models with either 17C7 or B5B5 to rule out the possibility that HHLA2-TMIGD2 axis contributes to the development of AML in vivo (Fig. 7d).