Fully differentiated and functionally specialized acinar cells of the rat pancreas are versatile and adaptable. Acinar cells can be stimulated to divide following administration of a mitogen or after inducing acinar cell necrosis. The degree of compensatory hyperplasia is dependent upon the extent of acinar cell necrosis. Type I injury (subtotal acinar cell necrosis) is followed by marked proliferation of acinar cells leading to complete restitution of the pancreas, whereas subsequent to type II injury (global acinar cell necrosis) there is no restitution of the pancreas because of lack of enough viable cells that have served as precursor cells. Associated with type Ii injury there is proliferation of ductular and periductular cells followed by the development of hepatocytes. In addition, during adverse conditions acinar cells undergo dedifferentiation and form pseudoductular structures. In rats, acinar tissue is a prime target for carcinogens. Transformed acinar cells form foci which are morphologically classified as acidophilic and basophilic lesions. Acidophilic foci which show increased cell proliferation progress to form nodules and acinar cell carcinomas.