In addition to TAA-induced cross priming and activation of CTLs, high dose irradiation’s ability to induce immunogenic tumor cell death also resulted from the activation of the cGMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway by cytosolic double stranded (ds) DNA from tumor cells post-irradiation, which resulted in increased type I interferon (IFN) expression, recruitment of DCs, and subsequent cross presentation and CD8+ T cell activation [36,37,38,39]. The gene discussed is STING1; the disease is neoplasm.