The third mechanism has been described in Hodgkin lymphomas (classical Hodgkin lymphomas and nodular lymphocyte-predominant Hodgkin lymphomas) and PMBL, in which both high JAK2 expression and p-STAT6 were observed and attributed to SOCS1 mutations via the disruption of a negative feedback loop [52,54,64]. The gene discussed is SOCS1; the disease is Hodgkins lymphoma.