It has been reported that COPB1-knockdown induced type I IFN signaling activation, leading to inhibition of Chlamydia psittaci intracellular proliferation (Li et al., 2025); pathogenic COPA variants cause chronic activation of the type I IFN signaling (Deng et al., 2020; Lepelley et al., 2020; Taguchi et al., 2021; Watkin et al., 2015); in iCCA targeting COPI activates STING-IFN-I pathway, triggering an anti-tumor T cell response. Here, PRRT2 is linked to neoplasm.