KM is thought to amplify adrenergic receptor-mediated cAMP signaling, as was demonstrated in C6 glioma cells [80], whereby Gαs-proteins were translocated from lipid rafts to non-raft-regions, allowing them to interact with and activate adenylate cyclase (AC), increasing cAMP production, even in the absence of G-protein receptor stimulation. Here, ASAH1 is linked to glioma.