EPO and stroke disorder: This observation is supported by cell culture and animal studies demonstrating that inhibition or gene knockdown of FoxO1 or FoxO3a results in stroke reduction by estradiol [91], protects against microglial cell demise during oxidative stress [106] and Aβ exposure [182], promotes the protective effects of metabotropic glutamate receptors [102], increases neuronal cell survival through nicotinamide adenine dinucleotide (NAD+) precursors [51], and provides trophic factor protection with erythropoietin (EPO) [28, 42, 46, 52] and neurotrophins [183–185].