We previously demonstrated that Fli1 deficiency contributes to the establishment of the pro-fibrotic phenotype in SSc fibroblasts and imatinib mesylate, which targets the c-Abl/PKC-δ/Fli1 pathway, reverses the pro-fibrotic phenotype of these cells [33,36]. The gene discussed is PRKCD; the disease is systemic sclerosis.