The combined results indicate that DLBCL cells, especially of the ABC subtype, appear to have evolved mechanisms that ensure STAT3 activation, through either the production of IL‐6 or the mutational inactivation of SOCS1. The co‐expression of gp130 and phospho‐STAT3 in patient biopsies lends further support to this hypothesis. This evidence concerns the gene SOCS1 and diffuse large B-cell lymphoma.