We further show that xenografted glioblastoma cells produced SPARC that both co-precipitated with Nogo-A and attenuated the binding of S1PR2 (Fig. 2i), whereas deletion of the Kazal-like module prevented SPARC from co-precipitating with Nogo-A, thus rescuing S1PR2 binding [Suppl. The gene discussed is SPARC; the disease is glioblastoma.