These results strongly suggest higher immunogenicity of RPM tumors, compared to RP lesions or subjects with a heterozygous loss of Msh2. Overall, WES analysis demonstrated that the homozygous loss of Msh2 in the RP background significantly increased the TMB, MMR mutational signature, and candidate neoantigenic load, resembling the MMR-defective subset of human SCLC (Liu et al. 2024). Here, MSH2 is linked to small cell lung carcinoma.