ATR and neoplasm: Additionally, ssGSEA analysis suggested that FAM111B positively influences DNA replication, G2M checkpoint control, DNA repair, and tumor proliferation pathways in LIHC, PAAD, MESO, and OV (Figure 5I–L, all p < 0.05), while GSEA analysis revealed FAM111B’s active role in DNA damage response pathways, including G1 cell-cycle control, the complete DNA repair network, DNA double-strand breaks, and ATR-mediated responses (Figure 5M–P; all p < 0.05).