In animal models, DFO treatment decreased AD hallmarks, iron overload, iron-induced kinase activity [cyclin-dependent kinase 5 (CDK5), glycogen synthase kinase 3β (GSK3β)], mitochondrial dysfunction, synaptic loss, and neuronal damage (Fine et al., 2012; Guo et al., 2013, 2015; Sripetchwandee et al., 2016). The gene discussed is CDK5; the disease is Alzheimer disease.