At this moment it can only be hypothesised that genes involved in immune cell signalling (such as SOCS2, UBE2N, and EPS15) could favour Th2 cytokine production to increase effector cells (eosinophilia and mastocytosis) and humoral response (high IgE levels) at the site of infection so individuals could become more resistant to gastrointestinal parasite infections. The gene discussed is SOCS2; the disease is mastocytosis.