This is presumably related to a reduced efficiency of antibody-dependent cellular cytotoxicity (ADCC) against HRS cells due to several alterations in signaling mechanisms in these cells and in the surrounding microenvironment, which act to promote tumor growth and immune evasion as well as rapid internalization and shedding of CD30 after ligand binding [16,17,18]. This evidence concerns the gene TNFRSF8 and neoplasm.