Infiltration with tumor-suppressive cells, downregulation of major histocompatibility complexes (MHC) class I molecules, and thus, hampered antigen presentation, apotosis inhibition by hypoxia, alterations in gut microbioma, defective tp53 and INF-signal pathways, amplified WNT/ß-Catenin, and TGF-ß signaling, inducing an increased portion of cancer stem cells (CSCs) that impact the tumor environment, are factors that promote to the tumor-mediated ICI bypass [9,10,20]. The gene discussed is CBLIF; the disease is neoplasm.