Observation of lysosomal abnormalities in brains from FTD patients with GRN mutations has led to the hypothesis that progranulin haploinsufficiency impairs lysosomal function, albeit less severely than complete progranulin deficiency, and that FTD-GRN may be on a continuum of lysosomal dysfunction with NCL due to GRN mutations [21, 25]. The gene discussed is NUCLEOLIN; the disease is hyperinsulinemic hypoglycemia, familial, 4.