Interestingly, this study defines a critical role for FBXL10 in DLBCL pathogenesis by activating a pro-survival ERK signaling pathway via transcriptional repression of DUSP6. Of note, DUSP6 is frequently inactivated in solid tumors and is specifically required for the dephosphorylation of ERK1/233,37. This evidence concerns the gene KDM2B and diffuse large B-cell lymphoma.