Previous studies have highlighted infection—particularly by Herpesviridae family viruses and certain bacteria—as a critical risk factor for BD, alongside genetic susceptibility.[12] The complement system is known to play a pivotal role in the immunological control of bacterial infections.[13] Through functional annotation and protein‐protein interaction (PPI) network analysis of proteins upregulated in severe BD, we found that complement components dominate the molecular pathways driving BD progression, with C4B emerging as the hub node in the PPI network based on degree centrality. The gene discussed is C4B; the disease is infection.