In addition, the accumulation of the neurotoxic substance δ-aminolaevulinic acid (δ-ALA) also contributes to the development of peripheral neuropathy.[11] The intermediates of tyrosine catabolism, maleylacetoacetate and maleylacetone (MA), are physiological substrates of GSTZ1. This evidence concerns the gene GSTZ1 and peripheral neuropathy.