Although JAK1/STAT3 mutants are oncogenic, they require lymphokine engagement (i.e. IL-6, IL-23) and JAK activation, whose inhibition (Ruxolitinib, HSP90) leads to STAT3 dephosphorylation, cell growth inhibition and lymphoma control in a Patient Derived Tumor Xenografted (PDTX) model. Here, STAT3 is linked to neoplasm.