A notable examplein this context comes from osteosarcoma, where only two out of fourcell lines had increased ERK phosphorylation to different extentsupon SEMA6D overexpression.9 Although PlexinA1 was reported as the receptor of SEMA6D, other cell-surface proteinssuch as vascular endothelial growth factor receptor 2 (VEGFR2), Off-Track(OTK), Ng-CAM related cell adhesion molecule (Nr-CAM), and PlexinA4 were also shown to interact with SEMA6D.2,3,8,11 Thus, differentialrepresentation of SEMA6D interacting proteins on the cell surfacecould also explain cell-specific effects that we observed. This evidence concerns the gene PLXNA1 and osteosarcoma.