To validate the potential role of KMT2A in the development of pulmonary fibrosis, we utilised AAV6 (adeno‐associated virus serotype 6) carrying three segments of Kmt2a gene shRNA sequences and designed a Col1a2‐specific promoter to achieve higher efficiency of infection in fibroblasts (Figure 2A,B).Western blotting results indicated that the expression of Collagen I was significantly down‐regulated in the lungs of mice treated with AAV6‐shKmt2a+BLM, while α‐SMA showed a decreasing trend but did not reach statistical significance (Figure 2G,H). Here, BLM is linked to infection.