Ascorbic acid can protect against stomach cancer by providing antioxidant effects on stomach cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosis, reducing the toxic effects of swallowed nitrosodimethylamines and heterocyclic amines, and preventing infections. Its eradication can restore vitamin C secretion by cutting the epithelium and allow regression of benign lesions of the stomach, interrupting the correlation cascade of gastric carcinogenesis. The levels of ascorbate in gastric juice depend on the absorption of ascorbic acid in the diet, but can also be reduced by infection, secretion of CAG, smoking, hydrochloric acid and chronic atrophic gastritis. Pilori can lead to the recovery of vitamin C from the stomach epithelium and allow the regression of pre-malignant stomach lesions. Routes of stomach carcinogenesis, virulence and interaction with antioxidants, vitamin C and phytochemical systems The mechanisms by which it interacts with other risk factors and protective factors, especially vitamin C in gastric carcinogenesis, are complex. There is evidence that ascorbic acid, phytochemicals and endogenous antioxidants can change the risk of developing stomach cancer. Other factors associated with vitamin C also play a role in stomach carcinogenesis. Stomach carcinogenesis includes metabolic, environmental, epigenetic, genomic, infectious, inflammatory and oncogenic pathways. The role of vitamin C in the epigenetic reprogramming of stomach cancer continues to develop. The molecular classification of stomach cancer subtypes has fundamentally changed the understanding of stomach carcinogenesis. Vitamin C is a class 1 carcinogen that causes chronic atrophic gastritis, gastrointestinal metaplasia, dysplasia and adenocarcinoma. By providing this information, we do not diagnose, treat, relieve or prevent any disease or condition. It is recommended to seek the advice of a licensed physician before starting any natural, integrative or routine treatment. This includes the microenvironment of the tumor, germ line mutations and the role of bacteria, viruses and epigenetics in somatic mutations.