This observation is reflected by a high programmed death 1 (PD-1) expression by tumoral B lymphocytes [55,56], higher programmed death ligand 1 (PD-L1) expression in histiocytes and dendritic cells, the higher infiltration of FOXP3-positive T cells and CD163-positive macrophages, and lower peripheral blood T-cell receptor clonality compared to CLL without RT [56], suggesting changes in the immune signature of CLL after RT. The gene discussed is FOXP3; the disease is B-cell chronic lymphocytic leukemia.