The Slc13a1 knockout mouse model exhibits hyposulfatemia and impaired growth, along with increased susceptibility to acetaminophen-induced hepatotoxicity and several other endocrine, neurodevelopmental, and reproductive phenotypes.10, 11, 12, 13, 14 Additionally, dogs and sheep found to have naturally occurring homozygous loss-of-function (LOF) variants in Slc13a1 exhibit hyposulfatemia and a form of osteochondrodysplasia characterized by growth restriction and angular deformities of the forelimbs.15 The gene discussed is SLC13A1; the disease is osteochondrodysplasia.