Considering that LTG is a VGCC blocker and that Ca++ influx has been reported to activate the PI3K/Akt axis in different cell systems [105,106,107], our results well fit with previously published reports showing that T-type Ca++ channel inhibition is able to interfere with mTOR/AKT pathway in a human lung adenocarcinoma cell line [108] and disrupted Akt signaling, promoting apoptosis, in glioblastoma cells [109]. Here, AKT1 is linked to glioblastoma.