Both NK and NKT-like cells are essential in the host's first line defense against viral infections and can produce antiviral effector cytokines including IFN-γ and TNF-α upon activation [19, 20].NK/NKT-like cell function is regulated by differential engagement of NK cell surface receptors (NKRs), which are divided into activation (NKp30, NKp44, NKp46, NKG2D, and NKG2C) and inhibitory (CD158a, CD158b, KIR3DL1, CD94 and NKG2A) NKRs [21–24]. This evidence concerns the gene NCR3 and viral infectious disease.