Inflammation is a manifestation of severe cellular injury, and the reaction tends to be stereo-patterned. The initial increased capillary permeability and the early migration of polymorphonuclear cells are pri- marily caused by a polypeptide to which there may be attached a prosthetic group. This substance, leucotaxine, has been identified. Leucotaxine fails to change the number of circulating leucocytes when injected intravenously. The leucocytosis is caused by a different basic factor (LPF) liberated by injured cells. The substance is thermolabile and nondiflusible. It can be extracted in the pseudoglobulin fraction of exudates. LPF induces a discharge into the circulation of immature granulocytes. It is absent from normal blood serum. LPF has a specific growth effect on some of the elements of the bone marrow. In an existing inflammation a single injn. of LPF induces a synergistic effect, so that the number of leucocytes remains elevated for markedly long periods. Injured cells also liberate a toxic substance called necrosin. Intravascular injn. of necrosin produces constant injury to the liver. This may be in the form of a stippling granulation in the hepatic cords, or the liver cells may display a prominent degree of vacuolation with scattered areas of leuco-cytic infiltrations. There may also be varying degrees of injury to the kidneys following necrosin injn. A fever-inducing factor called pyrexin has been dissociated from the true euglobulin fraction which is, or at least contains, necrosin. The pyrogen is thermostable and may have a central action. The leueo-penic factor of exudates seems to be closely associated with pyrexin and can be dissociated from the latter. This factor, which is probably liberated by injured cells, opposes the LPF in its mode of action. The leucopenic factor, which appears to be a polypeptide, seems to trap leucocytes in various organs. The facts presented show the necessity of studying thoroughly the biochemistry of cells injured previously by an irritant.