Additional contributors include dysfunctional circulating progenitors, fibroblast-derived anti-angiogenic mediators, and aberrant expression of transcription factors, such as Fos-related antigen-2 (Fra2) and Friend leukemia integration 1 transcription factor (Fli1), which may further contribute to SSc vasculopathy [62,63]. This evidence concerns the gene FLI1 and systemic sclerosis.