Interestingly, in keeping with overrepresentation of immune system processes amongst interactors of the EGFR PRM in U251 GBM cells, enriched pathways amongst these interactors included ‘inflammation mediated by chemokine/cytokine signalling’ and cholecystokinin receptor ‘CCKR’ signalling (Fig. 3dii). This evidence concerns the gene EGFR and glioblastoma.