Importantly, CD1a x CD3ε led to concentration-dependent T lymphocyte activation, as evaluated by up-regulation of CD69 and CD25 on both CD4 and CD8 T lymphocytes co-cultured with CD1a+ T-ALL, as well as by the release of granzyme, perforin, and granulysin, and the production of pro-inflammatory cytokines, such as TNF-α, IFN-γ, and IL-2 (Figure 3A–C). The gene discussed is CD4; the disease is acute lymphoblastic leukemia.