CBL and neoplasm: This additional checkpoint is mediated by common signaling molecules [e.g., c-Cbl, glycogen synthase kinase (GSK)-3β, diacylglycerol kinase (DGK)ζ, or cytokine-inducible Src homology-2 (SH2)-containing protein (CIS)] downstream of diverse activating receptors (1), which provides an additional strategy to enhance NK cell reactivity against tumor cells.