Brabetz et al., gained insights into AML progressions by using CRISPR to functionally study and “edit” the IDH2 genes to both create and correctively repair the mutation, IDH2 R140Q, frequently spotted in AML and are known to impede cellular differentiation and self-repair mechanisms (Brabetz et al., 2017). This evidence concerns the gene IDH2 and acute myeloid leukemia.