TGFB1 and acute myeloid leukemia: GSEA analysis indicated that the MYCMAX, VEGF, B‐cell receptor, NOTCH, MAPK, WNT and TGF‐beta signalling pathways were significantly upregulated in the IKZF1 N159S‐positive AML, while DNA mismatch repair and nucleotide excision repair pathways were significantly downregulated when compared with biCEBPA/‐like IKZF1 (Figure 2C).