We also found that deletion of signaling molecules that act upstream of type I IFN production including multiple TLRs (2, 3, 4, 5), RIPK2, cGAS/STING, or MAVS pathways, did not increase BMDM fusion during infection while control BMDMs lacking MyD88 and TRIF or IFNAR1 extensively fused (S1 Fig). Here, MYD88 is linked to infection.