In addition, there are two mouse models available for studying the function of the Oat and HOGA disease: a full KO line (Oattm1Dva) and a mouse line with a spontaneous recessive mutation, called retarded hair growth (Oatrhg), that harbors glycine-353 to alanine (G353A) substitution in OAT protein [150]. The gene discussed is OAT; the disease is ornithine aminotransferase deficiency.