In conclusion, assuming that CXCR5+TIM-3-PD-1+ T cells are as cytotoxic and stem cell-like in CRS as they are in other diseases, it is possible to intervene by targeting PD-1 to alter the exhaustion state of these cells, thereby modulating the cells’ capacity for sustained killing as well as their ability to self-proliferate and differentiate, and ultimately helping to terminate the continued progression of the disease. The gene discussed is PDCD1; the disease is congenital rubella syndrome.