Based on this finding, it’s possible that this treatment regimen could be further optimized to improve anti-tumor immunity, perhaps through the use of an IL-2 mutant “superkine” that preferentially binds and activates cytotoxic lymphocytes (CTLs) and NK cells (64), or a different interleukin, such as IL-15, that preferentially promotes the proliferation and activation of CTLs and effector T cells in comparison to Tregs (65). The gene discussed is IL2; the disease is neoplasm.