ATP1A1 and glioblastoma: Taken together, our study shows that when RB binds to ATP1A1, Na+-K+-ATPase is activated as a receptor, accompanied by activation of the intracellular MAPK/ERK pathway and inhibition of the Ca2+-regulated Src/FAK/Paxillin focal adhesion pathway, after which GBM cells undergo G2/M phase arrest and inhibition of invasion.