Many studies target shifting immune response from Th2 to Th1 immune response to control Trichinella spiralis as Del Prete et al. [57] who demonstrate that The Helicobacter pylori neutrophil-activating protein (HP-NAP) enhances endogenous IL-12 and IFN-γ response and exerts a powerful anti-T(H)2 activity in vivo, targeting both IL-5-induced eosinophilia and IL-4-mediated hyper-IgE responses induced by Trichinella spiralis infection. Here, IFNG is linked to trichinosis.