IFNAR1 and bacterial infectious disease: We have shown here that this extends to intracellular bacterial infection, with IFNAR signaling leading to the upregulation of genes important for enhancing a specific recruitment of selective autophagy, namely through Rnf31 (HOIP), Rbck1 (HOIL), and Lgals3bp. HOIP and HOIL are members of the LUBAC complex and, as such, play a vital role in marking cytosolic pathogens for removal by autophagy by depositing linear chains of ubiquitin on the surface of bacteria [40].