Given that inactivating mutations in upstream regulators of the RhoA pathway, including ARHGEF1, have been identified in primary GCB-DLBCL and BL26–28,40, our findings present an interesting model whereby fine-tuning the activity of the RhoA-ROCK pathway may be essential to prevent pathophysiology; aberrant activation of ROCK2 may promote ABC-DLBCL, while inactivation of this pathway may contribute to the pathogenesis of GCB-DLBCL or BL. Here, ARHGEF1 is linked to aneurysmal bone cyst.