Polymorphisms in ALDH3A2, ALDH4A1, ALDH5A1 and ALDH6A1 are associated with metabolic diseases accompanying neurologic complications [38–40] and inactivating mutations in ALDH3A2, ALDH4A1, ALDH5A1 and ALDH6A1 cause Sjögren-Larsson syndrome, type II hyperprolinemia, 4-hydroxybutyric aciduria and developmental delay, respectively [38, 41, 42]. This evidence concerns the gene ALDH3A2 and hyperprolinemia.