WITH the advent of new ideas and discoveries older theories gradually need revision as they become inadequate. Any departure from previous concepts should not be proffered in a spirit of dogmatism and should be most critically considered before being incorporated into even a working hypothesis. It is with this attitude that I wish to present a number of, what I think to be, concepts which differ in part from existing ideas in the study of underlying events in the production of necrosis in the living organism, There are so many phases of this problem that it will be impossible in such an abbreviated treatise to cover many of the controversial points, and again no single individual can be so imbued with knowledge as to adequately explain all the different phenomena in proper terms of chemistry, biology, physiology, and experimental and clinical data. It will be necessary, therefore, in great measure to depend on facts and opinions already presented by others. A number of dogmatic ide as must necessarily be presented without the proof of personal experiment, especially as it would require methods which will still have to be developed. Opinions here presented are the result of long consideration of what were thought to be better explanations of events, arrived at from copious laboratory, pathological, roentgenological, and clinical observations. Roentgenological findings, perhaps, offer much more important contributions in pathological diagnosis than is ordinarily thought, as changing events can often be much more conveniently followed roentgenographically than in the pathological laboratory. I doubt that any two pathologists would quite agree on what really constitutes “tissue necrosis,” even though the description of the gross and microscopic events of necrosis might be adecuately described. In the consideration of this subject the vast field of immunity must necessarily enter. Antibodies, opsonines, agglutinins, inflammatory reactions, allergy and all that it implies, all contribute to the process we wish to describe. In the discussion of tissue necrosis it is not my intention to describe the slow replacements such as we see in liver cirrhosis, secondary contracted kidney, etc., where the real functioning elements gradually degenerate and disappear under the influence of long-standing insults of numerous sorts. An entire organism or individual organs may suddenly cease to function, but such events do not constitute necrosis. Caustics may quickly destroy tissue as do other agents like extreme heat, chemicals, electricity, radiation, etc., but we shall not consider such in this paper. Neither shall this paper be concerned with the results of low-grade inflammatory reactions, where tissue destruction is a slow process varying in each case with variable and slowly changing conditions. We shall begin by considering acute inflammatory processes.