The pathophysiological process underlying asthma and CRSwNP is mostly driven by shared inflammatory mechanisms, which involve a complex activation of innate and adaptive immune cells, and increased production of several pro-inflammatory cytokines (e.g., interleukin (IL)-4, IL-5, IL-13, thymic stromal lymphopoietin (TSLP)). This evidence concerns the gene IL5 and asthma.