The complex network of effects involving autophagy in aging is also illustrated by the Zmpste24 deficient mouse, a model for human Hutchinson-Gilford progeria, a type of accelerated aging that exhibits autophagy induction, rather than reduction, in connection with metabolic changes, such as lower insulin and glucose levels in blood, thus rising a novel paradoxical role for autophagy during pathological aging processes [51, 52]. The gene discussed is ZMPSTE24; the disease is Hutchinson-Gilford progeria syndrome.