Comparison with certain processes in other portions of the body suggest the nature of this stimulus to organization in pneumonia. For example, it is well known that epithelial necrosis of the liver that results from chloroform is followed by a restitution of the organ to normal. On the other hand, if the liver necrosis is produced by a chemical agent plus a bacterial one, the destructive lesion not only involves the liver cell, but extends to the framework of the organ and terminates in a cirrhosis. Unquestionably, the difference between the reaction after the chemical alone and that after chemical plus bacterial injury is a more extensive destruction in the latter case resulting in a stimulation of all the elements of the organ, including liver cell, connective tissue, and blood vessel. The connective tissue and vascular elements have a greater capacity to regenerate than has the liver cell; consequently, granulations form which impede the less active reparative process of the hepatic cell. If this comparison be applied to the pulmonary changes in influenza and after the inhalation of poisonous gases, it will be seen that in both processes the initial damage is extensive, as has been indicated in the discussion of necrotization. Where the lesion is superficial, tracheal, bronchial, and alveolar epithelia rapidly regenerate and restore the injured surface. Where, however, the lesions are more extensive, alveolar and bronchiolar exudates are transformed into granulation tissue, even though the epithelium may manifest unusual activity in its attempt to repair a denuded area. VI. INFECTION AS A POSSIBLE ETIOLOGICAL FACTOR FOR MALIGNANT NEW GROWTHS