While our study focused on epithelial cells (A549/BEAS-2B) as the primary research model—driven by the central role of alveolar epithelial injury and EMT initiation in IPF pathogenesis—the observed in vivo suppression of macrophage-derived cytokines (IL-1β, MCP-1, IL-6) and collagen deposition suggests broader mechanistic implications. This evidence concerns the gene IL1B and idiopathic pulmonary fibrosis.