In addition, TGF-β1 levels were inversely correlated with the levels of granzyme B and IFN-γ release in WB following stimulation with P815-ULBP1+CD48 cells (granzyme B: p < 0.01; IFN-γ: p < 0.001) and K562 cells (IFN-γ: p < 0.01) (Figure 5C), implying TGF-β1 as a potential mediator of compromised NKA in MM. This evidence concerns the gene GZMB and Miyoshi myopathy.