Looking at the mutation states, such as TP53 and EGFR of LUAD cases, a significant enrichment of cell cycle- and mitochondrial function-related pathways was found in most samples, suggesting that UBR4’s pathological role is independent of specific oncogenic mutations in LUAD and in other lung cancer types as well (SI Appendix, Fig. S2 F and G). The gene discussed is TP53; the disease is lung cancer.