Specifically, PARPi-induced genetic instability has been shown to activate the cytosolic pattern recognition receptor cGAS and its associated pathway STImulator of Interferon Genes (cGAS-STING14) within the BRCA1-mutant cancer cells, resulting in the initiation of type I IFN production, cytokine-mediated T cell infiltration, and subsequent anti-tumor immune response11. This evidence concerns the gene CGAS and neoplasm.