Analyzing the expression of KIR receptor, CD158a, on NK cells and their CD3−CD56dim+ and CD3−CD56bright+ subsets, we show that, compared to treatment in CM, the percentage and MFI of this receptor do not change significantly (p > 0.05, Wilcoxon signed rank test) after 18 h in vitro treatments with all investigated cytokines in HC, as well as in MM patients (Figure 5a). This evidence concerns the gene KIR2DL1 and Miyoshi myopathy.