In this study, we found that RAB20 deficiency can activate NLRP3 inflammasome by promoting lysosomal disruption (25), simultaneous knockdown/knockout of RAB20 and NLRP3 in macrophage can effectively reverse SiO2-induced inflammatory factor release, but RAB20/NLRP3 double knockout mice must still be created to ensure the role of the RAB20/NLRP3 pathway in silicosis. This evidence concerns the gene RAB20 and silicosis.