Marmolino et al. conducted research that demonstrated how an azelaoyl PAF PPAR-g agonist, known as APAF (azelaoyl PAF), could increase expression of frataxin mRNA and protein in primary fibroblasts from both healthy individuals and Friedreich’s ataxia patients; similar effects were also observed with neuroblastoma cell line called SKNBE, suggesting that APAF might regulate the expression of the FXN gene in tissues relevant to disease [81]. The gene discussed is FXN; the disease is Friedreich ataxia.