Our data from cancer cell cultures confirm, indeed, that Pxl promotes a cGAS-STING pathway-dependent proinflammatory cascade, but they also show that Pxl treatment induces a strong upregulation of the PD-L1 protein in cancer cells in a cGAS-STING pathway-dependent manner (see Figures 3, 4). The gene discussed is CGAS; the disease is cancer.