In a model of silica-induced lung fibrosis, the prolonged activation of the NOD-like receptor protein 3 (NLRP3) inflammasome via the uncontrolled Shh/GLI and Wnt/β-catenin pathways facilitated the inflammatory microenvironment, including neutrophil, lymphocyte, and monocyte infiltration; the increased production of TNF-α and IL-1β; and enhanced EMT in the distal region [106]. This evidence concerns the gene SHH and pulmonary fibrosis.