Prior studies from our group and others had demonstrated that RT was capable of locally transforming an immunologically “cold” TME to one that is phenotypically “hot” through local activation of a type I interferon response via the cGAS/STING pathway, increased infiltration and activation of lymphocytes and dendritic cells in the radiated TME, upregulation of the major histocompatibility complex-I (MHC-I) and FAS expression on tumor cells, and the increased tumor expression of neoantigens (6, 24–30). The gene discussed is CGAS; the disease is neoplasm.