HIF1A and cancer: Indeed, silencing of uPAR expression or inhibition of uPAR interaction with integrins induces the inhibition of the PI3K/AKT/mTOR/HIF1 pathway, leading to impaired glucose uptake, decreased expression of various glycolytic enzymes and of PKM2, a checkpoint that controls metabolism of cancer cells; similar effects are also observed by silencing EGFR expression, suggesting its involvement in this uPAR activity [102].