Monti et al30 found that prenatal administration of N-acetyl-L-cysteine (NAC) to mouse fetuses with SLC26A2-associated diastrophic dysplasia via the drinking water of the pregnant females ameliorated the postnatal skeletal phenotype that results from the limited extracellular sulfate supply and subsequently reduced sulfation of macromolecules in the disorder. Here, SLC26A2 is linked to diastrophic dysplasia.