Furthermore, the underlying pathogenesis of PF is not yet fully understood; however, many mechanisms have been suggested, including prolongation of the local pulmonary inflammatory process, imbalance of pro-inflammatory/anti-inflammatory cytokines, exhaustion of the local pulmonary anti-oxidant system, augmentation of phosphodiesterase (PDE) activity, and provocation of epithelial/mesenchymal transition, which promotes the myofibroblast transformation, activation, and extracellular matrix deposition (2, 3, 5, 6). The gene discussed is ALDH7A1; the disease is pemphigus foliaceus.