In our study, the anti–PD-L1 Ab durvalumab demonstrated an antitumor immune response in CTCL by downregulation of both JAK/STAT and NF-κB pathways, driving PD-1+ M2-TAM polarization toward a more proinflammatory M1-like phenotype and inducing phagocytosis in vitro, which was enhanced by lenalidomide. The gene discussed is NFKB1; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.