Accordingly, a recent study showed that, within IL-2-activated NK cells, NKG2A+ cells degranulated more vigorously than NKG2A− cells against tumor cells with low HLA-E levels in a manner that was independent of KIR and HLA-I expression on NK and target cells, respectively, suggesting that better licensing by NKG2A overrides its inhibitory signaling, at least in these settings [88]. This evidence concerns the gene KLRC1 and neoplasm.