The purpose of this review was to describe the historical development of each epidemiology, experimental pathology, endocrinology (including vitaminology), and thermodynamics surrounding the genesis of gastric cancer in humans and non-human mammals. Epidemiological studies from other and our laboratories were unanimous in counting the intake of carbohydrate-rich and salty diet with vitamin C deficiency as the risk factor of key importance. Information from experimental pathology suggested the possible implication of some nitroso compounds in a subject with atrophic gastritis and/or in a state of vitamin C deficiency of which the establishment should have led to a perturbation of the steroid milieu of the host. In endocrinology, the association of a specific steroid disorder (depression of androgen and progestin combined with glucocorticoid excess in urine) with gastric cancer, as noted in the case-control study of this neoplasia, was reproduced in mice maintained under biased nutritional conditions. The use of scurvy-prone ODS rats was found useful in elucidating the interrelation between vitamin C and steroid metabolism. Finally, thermodynamic analysis of the data distribution of gastric cancer risk parameter of both sexes revealed the presence of an interaction between oncogene activation and tumor suppressor gene inactivation in the course of the maintenance of the positive correlation with male predominance between male gastric cancer and female gastric cancer as regards the changes of age-adjusted incidence rate (AAIR) in space. In conclusion, all of the information available in the field of gastric cancer etiology is in support of the pertinence of the steroid criminal hypothesis of gastric cancer in humans and in non-human mammals.