We found that primary IT disturbed the reversal of diabetes in recipients that received a sufficient mass of secondary transplanted islets, and a significant increase in CD69, TRAIL, and CXCR3 expression was observed in liver DX5− NK cells after secondary IT, in comparison with that in the control group that did not receive the primary IT, indicating their memory-like function. The gene discussed is TNFSF10; the disease is diabetes mellitus.