Similarly, the genetic modification of NK-92 cells to express a chimeric receptor with a TGFβRII extracellular and transmembrane domain, linked to an NK-activating NKG2D intracellular domain, exhibited resistance to TGFβ, a higher killing capacity, and elevated IFNγ production, as well as improved inhibition of tumor growth in vivo [137]. Here, TGFB1 is linked to neoplasm.