Gastric diseases are a heterogeneous group of disorders resulting from the complex interplay between environmental, genetic and microbial agents. These disorders may result from genetic or acquired factors, or a combination of both, and they can manifest in a variety of ways. Recent advances in molecular biology have allowed us to gain better insights into the molecular mechanisms underlying gastric diseases. At the cellular level, gastric diseases are associated with changes in the expression of genes involved in cell proliferation, apoptosis, inflammation and immune response. Dysregulation of these genes can lead to altered cell growth and survival, inflammation, and immune dysfunction. Additionally, changes in the expression of proteins involved in cell signaling, such as cytokines and chemokines, can affect the signaling pathways involved in the development of gastric diseases. At the molecular level, gastric diseases are associated with changes in the microbiome. Pathogenic organisms can cause inflammation and immune dysfunction, while beneficial bacteria can provide protection against disease.