RAG2 and neoplasm: By generating autochthonous tumors in Rag2−/− immunodeficient and Rag2+/− immunocompetent mice, and by performing complementary self vs. non-self tumor transplantation experiments, we observed that this therapeutic resistance was driven by reciprocal immunoediting and suppression of neoantigen expression in the tumor cells and by reshaping of the immune system during the development and progression of primary tumors.