Targeting OXPHOS de novo purine synthesis as the nexus of <i>FLT3</i> inhibitor-mediated synergistic antileukemic actions.

In line with this, sgRNAs for 28 genes in glycolysis (such as HK2 , HK3 , and PFKFB3 ) tended to be positively enriched in CRISPR screen of cell fitness to gilteritinib (although changes did not reach statistical significance) ( Fig. 4G and table S1) ( 20 ), implying that silencing these genes may provide survival benefit for gilteritinib-treated cells, which are adapted to OXPHOS and biosynthetic metabolism.

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