Patient samples from cHL have high expression of Pim-1,-2, and − 3 driven by NF-κB and STAT pathways and are sensitive to Pim kinase inhibition with the Pim/FLT3 inhibitor, SEL24/MEN1703 (SEL24-B489), or the dual Pim kinase combined with histone deacetylase inhibitor (suberoylanilide hydroxamic acid (SAHA) [130, 131]. Here, PIM1 is linked to classic Hodgkin lymphoma.