From the results of three independent experiments, we found that the inability to undergo autophagy during infection led to higher expression of many pro-inflammatory genes as compared to autophagy-competent cells, including established ISGs, such as Psmb10, Cd274, Cxcl10, Irf1 and Tap1 (Fig. 3a and Supplementary Table S1). This evidence concerns the gene TAP1 and infection.