We have previously proposed a model whereby arginine is rapidly depleted within an abscess due to its preferential uptake by host innate immune cells for inducible nitric oxide synthase (iNOS) (52), arginase (53, 54), and cell-mediated (55) immunity, effectively reducing the amount of free extracellular arginine available in the microenvironment. This evidence concerns the gene NOS2 and abscess.