NBIA often presents in children, but it can also present in late adulthood and this might be due to differences in genetic mutations (polymorphisms) [3]. One study found that patients who have mutations which lower the residual activity of the PanK2 enzyme are more likely to develop PKAN between the ages of one and six years [1]. The gene discussed is PANK2; the disease is neurodegeneration with brain iron accumulation.