SLC30A9 encodes a cation transporter thought to be primarily involved in cellular zinc homeostasis, designated ZnT-9.1 Recently, a novel syndrome consisting of a movement disorder, neurodevelopmental regression, oculomotor apraxia, and progressive renal impairment was described in a single large Bedouin kindred with a homozygous SLC30A9 in-frame deletion.2 A single individual from a second family with compound heterozygous variants has also very recently been reported.3 This condition has been designated Birk-Landau-Perez syndrome (BLPS).4 The gene discussed is SLC30A9; the disease is Oculomotor apraxia.