In fact, Fli1 has been previously described to function as a key regulator of the collagen homeostasis in the skin in vivo by repressing the collagen genes COL1A1, COL1A2, COL3A1, COL5A1 and COL5A2 [21] and has also been shown to be significantly reduced in clinically involved skin of patients with scleroderma [16]. The gene discussed is COL5A2; the disease is scleroderma.