We have shown that conditional PRKN expression results in prominent release of HMGB1 in the tumor microenvironment in vivo, and this pathway, combined with a limited release of mtDNA without overt mitochondrial damage (30), may converge to enhance STING- and IRF3-dependent IFN gene expression for PRKN tumor suppression. The gene discussed is IRF3; the disease is neoplasm.