Encouragingly, we demonstrated that both genetic silencing (Figure6A,B) and pharmaceutical inhibition with Runx1 specific inhibitor Ro5‐3335 (Figure 6C) on BMDMs effectively blocked TGF‐β1‐driven MMT formation in vitro, showing by the reduction of CAF morphology and marker expression (α‐SMA, FAP) in the 5‐day TGF‐β1‐stimulated BMDMs, suggesting Runx1 specific inhibitor can be further developed as a novel MMT targeted therapy for lung cancer. The gene discussed is ACTA1; the disease is lung cancer.