How does arginine deficiency translate into the physiological symptoms exhibited by patients with sepsis or other related diseases? Professor Juan Ochoa describes the cellular mechanisms that result in arginine deficiency and relates these to his observations in the clinic. First, he examines the actions of myeloid suppressor cells which express arginase-1. Following trauma, Ochoa divides the actions of myeloid cells into two classes. The M1 response increases nitric oxide levels, but the anti-inflammatory M2 response is what boosts the activities of arginase-1, resulting in rapid depletion of arginine levels.