TP53 and type 2 diabetes mellitus: As shown in Figure 3B, the GSEA revealed that glycolysis, MYC targets, Notch signaling, base excision repair, nucleotide excision repair, and p53 signaling pathway were significantly activated, whereas pancreas beta cells, ABC transporters, calcium signaling pathway, neuroactive ligand-receptor interaction, and type II diabetes mellitus were significantly inhibited in the high-risk group.