Although SIX1 has not been previously studied in lung fibrosis, an ovalbumin mouse model of asthma and a bronchial epithelial cell line (16HBE) showed that RNAi knockdown of Six1 decreased OVA-challenged inflammation, infiltration, and mucus production and that SIX1 siRNA-treated 16HBE cells suppressed TGF-β1–mediated epithelial-to-mesenchymal transition with a decrease in fibronectin and collagen IV expression (44, 45). Here, TGFB1 is linked to asthma.