The fact that, in our study, the induction of receptor-mediated mitophagy was more pronounced than ubiquitin-mediated mitophagy and that in vivo models of smoke exposure (or COPD) often describe activation of this PINK1/PRKN pathway (Ahmad et al., 2015; Ito et al., 2015; Mizumura et al., 2014), may be related to the fact that our in vitro models lack the inflammatory cells that are present in vivo in smoke-induced COPD. The gene discussed is PRKN; the disease is chronic obstructive pulmonary disease.