In addition, the molecular mechanisms by which high glucose promotes the over- expression of MUC5B as well as MUC5B promotes the activation of ERK1/2 are both unclear at present, which are needed to be studied in the future.In addition,the lack of further experiments to validate the implications of MUC5B site-specific mutation for the functions of BEAS-2B cells and for the aggravation of T2DM and ILD is also one of the limitations of this study. This evidence concerns the gene MUC5B and interstitial lung disease.