GSEA revealed that high-E2F neuroblastomas are significantly enriched in proliferative pathways, including cell cycle regulation (NES=2.89, p<0.001), DNA repair mechanisms (base/nucleotide excision repair: NES=2.35/2.24), and p53 signaling (NES=1.85) (Figures 4A–D), which is consistent with the established roles of E2Fs in driving cell cycle progression through direct transcriptional activation of cyclins and CDKs (15). This evidence concerns the gene TP53 and neuroblastoma.