Previously it was reported that mTORC2 and GSK3β have reciprocal activation in cancer including GBM.13 Upon Rictor knockdown, inhibitory phosphorylation of GSK3β at Ser9 was increased in U87MG cells and decreased in Rictor-overexpressed LN229 cells, as we have seen earlier (Figure 4a).13 Here we have addressed an obvious question whether mTORC2 plays as a master molecule in regulating the Hh pathway via GSK3β (Figure 4b). The gene discussed is GSK3B; the disease is glioblastoma.