Therefore, in this study, activating P38 MAPKs and NF-κB signaling pathways by the binding of Sp-CCAP to Sp-CCAPR were likely via cAMP and Ca2+ concentration changes in hepatopancreas cells, which promoted the expression of Sp-IL16, Sp-TNFSF, Sp-LYZ, Sp-ALF1, Sp-ALF4, and Sp-ALF5, hence enhancing the immune responses of S. paramamosain to pathogen infection. The gene discussed is IL16; the disease is infection.