In addition to our conclusions regarding the recruitment of TAM in GBM, we explored the impact of ERK1/2 signaling on two mechanisms that regulate the activation of TAM in solid tumors [7]: (1) high expression of PD1 ligands (PD-L1 and PD-L2) in GBM cells and (2) the secretion of lactate combined with high expression of the gene encoding its receptor GPR65, recently found to be an essential contributor to the noninflammatory polarization of TAM [16]. The gene discussed is MAPK3; the disease is glioblastoma.