To gain further biological insights into the underlying mechanisms of RhoF overexpression in AML, GSEA analysis was performed and revealed that the gene sets were significantly enriched in MYC targets (NES =3.79, P <0.001), P53 pathways (NES =3.21, P<0.001) and E2F targets (NES =3.09, P<0.001) (Figure 7F-H). The gene discussed is TP53; the disease is acute myeloid leukemia.