AKT1 and neoplasm: Together, these findings raise a possibility that in the course of tumor progression, cancer cells upregulate the expression of ILK in response to microenvironmental stimuli, such as hypoxia and inflammatory cytokines, to gain growth advantage and metastatic capacity mediated through various downstream signaling effectors, including Akt, GSK3β, and YB-1 [23], [32], [65], [66].