In this study, we confirmed that SDF-1 could amplify the role of EX-4 by significantly activating metabolism-related signaling pathways, such as type II diabetes mellitus and insulin signaling pathways; and EX-4 could aggravate the effect of SDF-1 on PDLSCs biological roles by regulating primary immunodeficiency and tight junction signaling pathways. This evidence concerns the gene INS and inborn error of immunity.