Conversely, a population of low-avidity CD8+ T cells will exhibit multifaceted failure: motile targets will escape inefficient engagement, permitting viral replication and spread, while upon killing a target, weak TCR signaling and secretion of low quantities of β-chemokines insufficient for blocking new infections might recruit additional CD4+ cells to the tissue, thereby inadvertently promoting rapid viral replication [2]. The gene discussed is CD8A; the disease is infection.