In this context, the activating receptor NKG2D that recognizes stress-induced cellular ligands often overexpressed upon viral infection or tumor transformation (i.e., MIC-A, MIC-B, and ULBPs) (Lanier, 2015), is central in NK-mediated immune responses against virtually all Herpesviruses, namely HSV-1, VZV, CMV, HHV6, HHV7, KSHV, and EBV, all of which encode molecules downregulating NKG2D ligands (Wu et al., 2003; Thomas et al., 2008; Nachmani et al., 2009; Schneider and Hudson, 2011; Campbell et al., 2015; Schmiedel et al., 2016). Here, KLRK1 is linked to neoplasm.