Glioblastoma (GBM) is the most common and malignant primary brain tumor. Non-muscle myosin II (NMII) paralogues (NMIIA, IIB and IIC) have multiple roles in normal cell physiology, but also contribute to pathological states, including GBM. Because oncogenic kinase inhibitors often fail in GBM due to pathway redundancy, targeting NMIIs, which are common downstream effectors, may offer a more effective strategy.