All incubated NK cell samples from the five HNSCC patients exhibited a time-dependent down-regulation of NKG2D expression on total NK cells and both NK cell subsets (Figures 2A,B), whereas surface expression of CD16, pro-apoptotic FasL, and TRAIL receptors as well as activation marker CD57 were largely unaffected and stable over the indicated time period on all NK cell fractions by the described sMICA analogs (Figure 3A). The gene discussed is KLRK1; the disease is head and neck squamous cell carcinoma.