Hence, these observations motivate us to investigate the physiological role of lipid raft membrane-associated PI3K-Rac1-Akt effector molecules in modulating the GLUT-1-mediated glucose and lipid metabolism of the invasive potential of TSC cells, and to determine the molecular mechanism about how GA-induced CK2 activation affecting cell invasion. Here, SLC2A1 is linked to tuberous sclerosis.