PEX2 and peroxisomal disease: Another explanation for why no ER stress and UPR activation was observed in peroxisome-deficient CHO cells, in contrast to, e.g., postnatal Pex2–/– mouse tissues or biopsies obtained from patients with peroxisomal disorders (Kovacs et al., 2009, 2012; Launay et al., 2017), might be the lack of accumulation of ER stress-inducing metabolites.