The latest research shows that patient derived individual mutations in the NF2 FERM domain can convert NF2 into potent inhibitors of cGAS-STING signaling: activated IRF3 can directly bind to and induce mutant NF2 to form cell aggregates, which significantly reduces immune cell infiltration, especially CD4+and CD8+T lymphocytes, thereby eliminating STING induced anti-tumor immunity (124–126). Here, STING1 is linked to neoplasm.