To begin to assess whether heightened rac activity contributed to the enhanced fibrotic phenotype of lesional SSc fibroblasts, we used real-time PCR analysis to show, as expected, that α-SMA, type I collagen (COL1A2), vinculin and CTGF mRNAs were elevated in SSc dermal fibroblasts (SScF) compared to control fibroblasts (NF) (Figure 2A). This evidence concerns the gene COL1A2 and systemic sclerosis.