Interestingly, Murray et al. [25] showed that when L. donovani, which causes visceral leishmaniasis, is used to infect the same WT, TLR2−/− and TLR4−/− mice as used in our study, a contrasting role for the two TLRs is found whereby a lack of TLR2 leads to enhanced and sustained reduction in parasite replication in the liver, whilst a lack of TLR4 leads to increased parasitaemia at the peak of infection. The gene discussed is TLR4; the disease is visceral leishmaniasis.