Our study confirmed that SDF-1 could amplify the role of EX-4 by activating more metabolism-related signaling pathways, such as type II diabetes mellitus and the 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 type 2 diabetes mellitus.