Most interestingly, MiSL identified BCL2L2 (Bcl-w) as a candidate SL partner of the IDH1 mutation: IDH1 mutation and BCL2L2 deletion were mutually exclusive (HI-LO Boolean implication) in the TCGA data; BCL2L2 deletion resulted in lowered expression, so BCL2L2 is unlikely to be a passenger deletion; and BCL2L2 was differentially overexpressed in IDH1-mutant compared to IDH1-wild-type AML (Fig. 2h). This evidence concerns the gene IDH1 and acute myeloid leukemia.