Recently we published evidence that continued activation of STAT5 plays a role in the lymphomagenesis of classical Hodgkin Lymphoma [17] . We showed that long-term culture of primary B cells expressing constitutive active STAT5 mutants eventually led to a phenotype closely resembling classical Hodgkin Lymphoma cells, including the loss of immunoglobulin expression and other B cell specific markers as CD20 [29, 30, 31] . The absence of immunoglobulin expression is an important hallmark of classical Hodgkin lymphoma [32] . In approximately 25% of the cases mutations leading to a crippled immunoglobulin expression can be found [32, 33] . However, in the majority of the cases no crippled mutations can be found and epigenetic events on the promoter region of the immunoglobulin heavy chain have been proposed as an alternative explanation for the absence of immunoglobulin expression by Hodgkin Lymphoma cells [28] .