In GSEA analysis using the c2 gene set, we found that high-risk AML patients were notably enriched in the following signaling pathways: NF/kappa B, VEGF, Toll-like receptor (TLR) pathway, Notch, tumor protein 53 (TP53), apoptosis, TCR, Akt1, mitogen-activated protein kinase (MAPK), Wnt, tumor necrosis factor (TNF), AML cluster 15, B-cell receptor (BCR) signaling pathway, and cytokine-cytokine pathway (Fig. 7A–P, Table S6). The gene discussed is AKT1; the disease is acute myeloid leukemia.