Sources of ROS and regulation cellular redox homeostasis in hematopoiesis. Ionizing radiation (IR), ultraviolet (UV), chemical drugs, etc. result in exogenous elevated ROS levels. Accumulated O2- molecules by mitochondria and membrane NADPH oxidase (NOX) in cells are first converted by superoxide dismutase (SOD) into H2O2. H2O2 quickly converts into harmless water (H2O) in the presence of catalase, glutathione (GSH), glutathione peroxidase (GPX), peroxiredoxin (PRX), and thioredoxin (TRX). If cells are insufficient to detoxify H2O2, the remaining H2O2 is converted into even more toxic OH- ions. OH- ions can lead to destruction of cellular macromolecules including proteins, nuclear acids, and lipids. N-acetyl cysteine (NAC) and resveratrol are two small molecule antioxidants which reduce ROS levels. In hematopoiesis, dormant, quiescent HSCs are characterized by low ROS levels. Elevated ROS levels in HSCs enhance cycling and promote differentiation and mobilization.