With the downstream targeting of JAK2, the persistent activation of STAT3 in primary exudative lymphoma (PEL) and large granular lymphocytic leukemia (LGL) has been revealed, where approximately 40% of LGL subtypes have increased STAT3 activity and are used as a diagnostic marker of LGL [19, 20], implying that, to a certain extent, targeting the JAK2/STAT3 signaling pathway for lymphoma therapy is reasonable. This evidence concerns the gene STAT3 and primary effusion lymphoma.