Thus, the loss of mDia1 and mDia2 protein expression observed in response to sustained IMM02-induced global mDia agonism could be considered broadly as an “event-driven” pharmacologic strategy [45] that could reasonably be used to alter the molecular and functional cellular phenotypes in our GBM patient-derived cell line experimental system. The gene discussed is DIAPH3; the disease is glioblastoma.