Similarly, we demonstrated the relevance of the genetic background of C57BL/6 and BALB/c mice strains in tolerance mechanisms during YFV17D infection, suggesting that increased expression of H2-T23 (Qa-1/HLA-E) and FOXP3 transcripts in thymus and liver of C57BL/6 mice, together with a defective control of viral load, might be indicative of a higher susceptibility of this strain to YFV17D infection. The gene discussed is FOXP3; the disease is infection.