PLEK2 could interact with the kinase domain of EGFR and suppress EGFR ubiquitination mediated by c‐CBL, leading to constitutive activation of EGFR signaling.[327] GBM with higher EGFR levels displayed higher expression of vascular cell adhesion molecule‐1 (VCAM‐1), mediated by the p38/STAT pathway[328] or through protein kinase (PKC) and NF‐κB,[329] thereby promoting macrophage infiltration and glioblastoma invasion. The gene discussed is CBL; the disease is glioblastoma.