This finding indicated that AFP stimulated the cleavage of membrane MICA/B in HCC cells, increased the content of soluble MICA/B, and blocked the interaction between MICA/B and NKG2D, which may be involved in the upregulation of MMP9 expression via activation of the PI3K/AKT signalling pathway. The gene discussed is AKT1; the disease is hepatocellular carcinoma.