Next, we found that δ-TT treatment leads to a specific decrease in HK2 protein levels in PTEN-null PCa cells, without altering the expression of other key glycolytic enzymes, including GLUT1, PKM2 and LDH-A; as expected, these changes were followed by a significant reduction in glucose consumption and lactate production. The gene discussed is SLC2A1; the disease is posterior cortical atrophy.