However, in a LKB1 (liver kinase B1)- and AMPK-deficient mouse model of Peutz-Jeghers syndrome, there is up-regulation of mTOR (mammalian target of rapamycin) and HIF-1 (hypoxia-inducible factor 1) α transcription factor that leads to higher hexokinase II and Glut1 expression and increased glucose utilization by the tumours [26]. Here, SLC2A1 is linked to neoplasm.