Furthermore, we presented a proof‐of‐concept example that deletion of CB1R, an upstream regulator of IRF5,[29, 30] attenuated pathological changes in G‐0, G‐1, and G‐2 subnetworks in the GCN of fibrotic lung transcriptome, underscoring its potential as an emerging therapeutic target for PF treatment (Figures 8A–E and 7C). Here, IRF5 is linked to pemphigus foliaceus.