Eric S Yvon et al. revealed that the function of UCB-derived NK cells including the ability to kill glioblastoma tumor cells, the secretion of IFN-γ and perforin, and the expression levels of NKG2D/DNMA1, were maintained in the presence of TGFβ via engineering a dominant negative TGFβ receptor II into them (59) (Figure 1). Here, KLRK1 is linked to neoplasm.