Second, the (IIB) functional loss of tumor-suppressive genes such as phosphatase and tensin homolog (PTEN) in glioma, and the loss of Lkb1 (also known as serine-threonine kinase 11 [Stk11]) and PTEN in squamous cell carcinoma of the lung, results in the activation of the phosphatidylinositol-3-OH kinase (PI3Kinase) pathway, then the activation of the AKT pathway, followed by the PD-L1 promoter; thus, the expression of the PD-L1 protein seems to be dependent on Akt activation in some cases of glioma [38] and lung cancer [39]. This evidence concerns the gene AKT1 and lung carcinoma.