TMEM160 inhibits the degradation of PD‐L1 that, in turn, fosters the malignant progress, radio‐resistance and immune evasion of CRC cells [41], while VKR‐2 is a kinase effector of signaling pathways that regulate apoptosis and tumor cell growth, also through PD‐L1 network [42]. Here, TMEM160 is linked to neoplasm.