This may be attributed to the following three reasons: 1) the distinct interactions of COL3A1 mutations with CTLA-4 and PD-1/PD-L1, for example, synergistic and antagonistic roles; 2) the tumor microenvironment may be distinctly influenced by the two ICI treatments, which would generate differential immunogenicity in patients with COL3A1 mutations; and 3) the sample size used for the two ICI types (324 vs. 158) may also be a potential reason for the distinct survival differences. This evidence concerns the gene PDCD1 and neoplasm.