In summary, microbial infection, autophagy regulated by PI3K/Akt pathway, inflammation modulation related to NF-κB, TGF-β, and MAPK pathways were critical for disease development in AS; function of the ubiquitin–proteasome system and regulation of NF-κB and Wnt pathways were important for BD; activation of retinoic acid-inducible gene-I (RIG-I)-like receptor (RLR) signaling pathway, function of ER and NETs were vital for SCL; apoptosis, regulation of MAPK and JAK pathways and the effect of protein phosphatase were critical for VKH. Here, DHX58 is linked to Behcet disease.