To mitigate the adverse effects of TGF-β, Yvon et al. used UCB as a source of allogeneic NK cells with a genetically modified dominant-negative TGF-β receptor II and verified that they could sustain both NKG2D expression and release of IFN-γ in the presence of TGF-β for the identification and lysis of GBM cancer cells [62, 73, 74]. Here, KLRK1 is linked to glioblastoma.