According to GSEA, the low-risk group was primarily influenced by pathways related to the TCA cycle, DNA replication, nucleotide excision repair, oxidative phosphorylation, and RNA degradation (Figure 6E), while the high-risk group was particularly impacted by autoimmune thyroid disease, cytokine-cytokine receptor interactions, the JAK–STAT signaling pathway, and natural killer cell-mediated cytotoxicity (Figure 6D). Here, SOAT1 is linked to autoimmune thyroid disease.