After exposure to irradiation or oncogenic transposons, cGAS- and STING-deficient mice show decreased upregulation of SASP factors like interleukin 6 (IL-6), C-X-C motif chemokine ligand (CXCL) 10, and cyclin dependent kinase inhibitor 2A (Cdkn2a) in vivo.21 Furthermore, nuclear programmed death-ligand 1 (PD-L1) silencing in the lung cancer A549 cell line enhances STING promoter activity, upregulates STING expression, induces tumor cell senescence, and inhibits lung cancer growth. The gene discussed is CGAS; the disease is neoplasm.