In classical Hodgkin lymphoma, the PI3Kδ-specific inhibitors GS-1101 [17] and Auranofin [69] and the NF-κB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) [70] not only were cytotoxic, but also decreased CCL5 secretion by cancer cells, leading to a reduced capability to recruit peripheral blood mononuclear cells (PBMCs) [69]. The gene discussed is CCL5; the disease is cancer.