Infection with Helicobacter pylori (H. pylori) is prevalent around the world and responsible for gastric cancer (GC). The development of GC from gastritis is closely associated with the bacterial virulence and the body's immune response ability. In this process, interleukin-1β (IL-1β) plays an important role. Under H. pylori infection, IL-1β is highly expressed that result in gastric acid inhibition, GC-related gene methylations and disfunctions, angiogenesis. Nod-like receptor pyrin domain containing 3 (NLRP3) inflammasome mediates IL-1β maturation in cells such as macrophages, neutrophils and dendritic cells. But how does IL-1β get released across the cell membrane still unclear. In this review, we focus on the secretion mechanism of IL-1β across the membrane, and to explore the role of IL-1β in the progression of GC.