STAT3 and primary cutaneous T-cell non-Hodgkin lymphoma: HDACs are implicated in a wide range of cellular processes [21–23] including JAK2/STAT3 signaling pathway inhibition through regulation of suppressor of cytokine signaling proteins (SOCS), a family of genes involved in JAK2-STAT3 signaling pathway inhibition [24, 25], while they are also highly upregulated in CTCL [26] and in B- and T- cell lymphoma patients [27].