Supporting this hypothesis, exogenous ET-1 did not affect type I collagen expression, whereas bosentan suppressed the expression of c-Abl and PKC-δ, decreased the nuclear localization of PKC-δ and Fli1 phosphorylation at threonine 312, and eventually increased the DNA binding ability of Fli1 to the COL1A2 promoter resulting in the reduction of type I collagen expression in SSc dermal fibroblasts. The gene discussed is ABL1; the disease is systemic sclerosis.