A comparison of the stoichiometry (96, 150, 151) of NMBR occupation, mobilization of cellular calcium, generation of phosphoinositides, activation of phospholipase D, and stimulation of p125 FAK tyrosine phosphorylation, between NMBR activation on rat C-6 glioma cells and human NMBRs in a normal cell, showed results that were superimposable, and furthermore, the degree of receptor spareness in NMBR occupation and activation of the different signaling cascades was similar, demonstrating the NMBR on these tumor cells and NMBR in human cells had identical signaling coupling (Figure 1). The gene discussed is PTK2; the disease is glioma.