[72] (another TARGET initiative study on paediatric AML) employed whole‐genome and RNA sequencing found that AML groups with genetic clones bearing initiation mutations such as NUP98‐NSD1 collude with mutations in FRMD8, WT1 and others to prevail and may correlate with causing chemoresistance, whereas subclones with mutations in FLT3 and NRAS were eradicated by chemotherapy and thus are not associated with disease relapse after chemotherapy. This evidence concerns the gene NRAS and acute myeloid leukemia.