The significant overlap of cell signaling pathway and transcripts controlled by the mRNA-binding protein HuR with transcripts essential for stress-responsive TREM1 activation, myeloid-derived cell directional migration, and fusion creates the unique opportunity to override the TREM1-dependent complex myeloid-derived glioblastoma microenvironment with a recently discovered BBB permeable HuR inhibitor.11–13,27–31 Our current work explores the oncogenic role of the TREM1+-myeloid-derived glioblastoma microenvironment and presents a novel pharmacological opportunity for its inhibition. The gene discussed is TREM1; the disease is glioblastoma.