Huang et al. reported that the global hypermethylation in IPF patient myofibroblasts caused silencing of the prostaglandin receptor E2 (PTGER2) gene and proposed that methylation of this gene contributed to the myofibroblast phenotype[13] while Hagood et al. have provided evidence of Thy-1 methylation contributing to such differentiation[15]. The gene discussed is THY1; the disease is idiopathic pulmonary fibrosis.