Studies in chronic smokers and COPD patients have shown that ER stress and UPR activation have occurred by measuring relevant markers, including GRP78, PERK, eIF2α and CHOP, indicating a possible role of ER stress and prolonged UPR activation that result in cell death and COPD (Malhotra et al., 2009; Geraghty et al., 2016). The gene discussed is EIF2A; the disease is chronic obstructive pulmonary disease.