Potential mechanisms by which cGAS/STING activation enhances the efficacy of anti-PD-1/PD-L1 therapies include increasing T-cell infiltration in the tumors and/or reducing tumor-associated myeloid cells (5), elevating expression of MHC class I and tumor cell recognition by T cells (6), and enhancing the function of antigen-presenting cells, natural killer (NK) cells, and T cells (7–9). The gene discussed is CGAS; the disease is neoplasm.