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). The gene discussed is AKT1; the disease is systemic sclerosis.