In particular, engineering with the IL-2 cDNA allowed robust amplification of T cells in the long term.64,65 The development was dropped, however, since IL-2- or TNF-α-modified TILs did not show clinical benefit over nonmodified TILs.66 Evidence reported by the Sadelain group52 indicated that IFN-γ and IL-2 release upon redirected activation of patients' T cells was increased when the targeted cancer cells express CD80, the ligand for CD28 on T cells. The gene discussed is CD28; the disease is cancer.