PEX26 and Zellweger syndrome: Loss-of-function variants of PEX1, PEX6, or PEX26 were shown to completely impede matrix protein import and thus abolish all peroxisomal metabolic functions by disturbed recycling of the peroxisomal PTS1 receptor resulting in the clinical phenotype of ZS (Geisbrecht et al., 1998; Matsumoto et al., 2003b).