STAT6 and neoplasm: The mutational landscape of rrDLBCL tumors remains largely similar to ndDLBCL, although enrichment for low frequency mutations such as MS4A1 (3.4% vs 0.5%), CD79A (3.9% vs 1.0%), or STAT6 (7.8% vs 3.7%) suggest mechanisms of resistance to anti-CD20 driven therapy, constitutive activation of B-cell receptor signaling, and remodeling of the tumor microenvironment are highly specific features in a subset of DLBCL tumors refractory to immunochemotherapy [24, 25, 51, 52].