As indicated by recent studies, UCA1 activates mTOR by upregulating HK2 and increases glycolysis through both the activation of STAT3 and the repression of miR-143, thereby revealing a novel glucose metabolism regulatory pathway, UCA1-mTOR-STAT3/miR-143/HK2, in bladder cancer cells [131, 132]. This evidence concerns the gene HK2 and urinary bladder carcinoma.