Furthermore, it was revealed that specific intratumoral regions maintained functional connectivity by thrombospondin/thrombin sensitive protein 1 (TSP‐1)‐expressing malignant cells subpopulation (high functional connectivity (HFC) GBM cells), suggesting that pharmacological suppression of TSP‐1 reduces glioblastoma cell growth and network synchrony in TME and highlighting an efficient therapeutic strategy for future clinical research.42 The gene discussed is THBS1; the disease is glioblastoma.