These data suggest that PERK is a major participant in the transcriptional control of ATF6 and many UPR target genes in response to tunicamycin treatment in X-ALD fibroblasts, including those involved in protein folding, such as GRP94 or GRP78 and ERAD factors such as EDEM2 or HERPUD1. This evidence concerns the gene ATF6 and X-linked adrenoleukodystrophy.