High expression of MIF in tumors activates the PI3K/AKT pathway via interactions with CD74 and CXCR7 [53], thereafter inhibiting NR3C2 [32], p53 [33] and p27 [54] expression and upregulating downstream targets, including cyclin D1, cyclin-dependent kinase (CDK), MMP-7, c-Myc, c-Jun, MMP-9 and VEGF [55–57], thus promoting tumor growth, metastasis and survival while inhibiting apoptosis. Here, AKT1 is linked to neoplasm.