RANKL inhibition in vivo, including the use of a soluble RANK-Fc molecule, does not prevent the priming of LCMV-specific T cells, but it has damaged effects on proliferation of CD4+ T cells to the viral antigen after a period of infection, reaching a point at which RANKL seems to play a role in memory T-cell responses (153). The gene discussed is TNFSF11; the disease is infection.