Knockdown of pro-fibrotic miR-26a, which was predicted to target the FLI1 untranslated region, increased Fli1 expression and decreased collagen I and fibronectin expression in SSc skin fibroblasts, while miR-26 transfection reduced the Fli1 level and enhanced collagen I and fibronectin accumulation [31]. The gene discussed is FN1; the disease is systemic sclerosis.