The proteomic analysis suggested strong interaction of Cur with p53, PAI-I, and uPA proteins as an expression of IL-17A-mediated inflammation in the impairment of the p53-fibrinolytic system and alveolar epithelial cell (AEC) apoptosis, which is a critical pathophysiological hallmark of pulmonary fibrosis. This evidence concerns the gene TP53 and pulmonary fibrosis.