In contrast, α-SMA, CTGF, and NF-κB were reduced by rosiglitazone treatment to a similar extent in SSc-ILD fibroblasts derived from either black or white subjects, suggesting that the PPARγ agonist reduces α-SMA, CTGF, and NF-κB by a mechanism(s) independent of HGF. Here, NFKB1 is linked to interstitial lung disease.