Patients with loss-of-function mutations in ZIP14 developed severe childhood-onset neurological disorders due to manganese accumulation in the brain; similarly, mice with whole-body Zip14 knockout displayed manganese loading in the blood and brain at over 10 times the normal level, indicating an indispensable role for ZIP14 in maintaining systemic manganese homeostasis [18,19,21,22,23,24,25]. Here, SLC39A14 is linked to nervous system disorder.