Importantly, these results are substantiated by the study of the expression of AMACR, ACOX3 and DBP in human prostate samples, showing a specific and consistent overexpression of proteins involved in peroxisomal fatty acid oxidation in PCa as well as in PIN lesions in contrast to benign tissue, suggesting a possible aetiological role for this pathway in malignant transformation. Here, AMACR is linked to posterior cortical atrophy.