To further determine whether neuronal IFN-I signaling is responsible for the acute antinociceptive effects of STING agonists, we established the bone cancer pain model using mice lacking Ifnar1 selectively in sensory neurons (Ifnar1fx/fx; Nav1.8-Cre; Ifnar1-cKO), or their wildtype littermates. The gene discussed is STING1; the disease is bone cancer.