Consistent with this model, loss of Kmt2d alone in the GC was not sufficient to drive lymphomagenesis, but when combined with deregulated expression of BCL2 (as observed in human FL and DLBCL) the two cooperate, leading to a significant increase in the percentage of bona fide FL and DLBCL characterized by clonally rearranged, mutated IGHV genes and the expression of GC-specific markers (Figure 3C) (41). The gene discussed is KMT2D; the disease is diffuse large B-cell lymphoma.