Collectively, our findings strongly support a model of E2F1, MYB, STAT1 and FLI1 being important regulators of the postnatal ontogeny of Mo immunometabolism with high E2F1 and MYB expression in NEO Mo promoting OXPHOS and cell differentiation that shifts to low E2F1 and MYB expression and high STAT1 expression with increasing age, driving glycolysis and inflammatory activity in AD Mo in liaison with FLI1. The gene discussed is FLI1; the disease is Alzheimer disease.