We noted a selective reduction in cell viability with the small molecule 5-(tetradecycloxy)-2-furoic acid (TOFA), a selective competitive inhibitor of acetyl-CoA carboxylase 1 (ACACA)35, which MiSL predicted to be a SL partner of the IDH1 mutation in AML: there was a strong HI-LO Boolean implication between IDH1 mutation and ACACA deletions in the pan-cancer TCGA data with zero overlap between the two events, ACACA deletions resulted in lowered expression of ACACA, and ACACA was differentially overexpressed in IDH1-mutant AML compared to IDH1-wild-type AML (Fig. 3c). The gene discussed is ACACA; the disease is acute myeloid leukemia.