Since terminal differentiation requires B-cells to transition from a highly activated state to a plasmacytic phenotype, these findings suggest that ROCK2 may support the PB-like features of ABC-DLBCL by promoting the expression of pathways that allow for the maintenance of proliferation and survival while repressing components of the B-cell activation program, such as BCR signaling and co-stimulation. The gene discussed is BCR; the disease is aneurysmal bone cyst.