Since the immune microenvironment mediates ICB responses, we further analyzed the differences in ICB response signatures between high and low-risk groups and found that in the low-risk group, Systemic lupus erythematosus, Viral carcinogenesis, Base excision repair, p53 signaling pathway, Proteasome, and microRNAs in cancer risk scores were higher in the low-risk group than in the high-risk group, and there were no significant differences in other ICB response signatures (Figure 9E). The gene discussed is TP53; the disease is systemic lupus erythematosus.