In glioblastoma, EGFR and EGFRvIII cooperate to induce macrophage attraction via upregulating CCL2, with KRAS serving as a critical signaling intermediate.[325] CCL2 expression is also increased in EGFR‐ and/or HER2‐positive breast cancer, leading to increased TAM recruitment and motility.[326] CCL2 is a target gene downstream of pleckstrin‐2 (PLEK2) /EGFR signaling, promoting TAM infiltration and tumor cell growth. This evidence concerns the gene PLEK2 and glioblastoma.