Since 20F2 could selectively block the HHLA2-independent TMIGD2 signaling in AML cells but largely maintain costimulatory signaling mediated by HHLA2-TMIGD2 interaction on T and NK cells (Supplementary Fig. 7h, i), which is potentially better than 17C7, we treated more AML PDX models that were established with hard-to-treat or secondary AML patient samples (Pt#19, Pt#8 and Pt#24), and found that all responded well to 20F2 therapy (Fig. 7i). The gene discussed is TMIGD2; the disease is acute myeloid leukemia.