Studies have shown that tumor cells may shed or otherwise restrict the presentation of NK‐cell receptor D (NKG2D) ligands, such as MICA, MICB, and ULBPs, involved in their recognition by NK cells or cytotoxic T lymphocytes (CTLs), or downregulate the expression of other factors that promote the activation of tumor‐specific immune responses.62, 63, 64, 65, 66, 67 Furthermore, it is established that tumor cells that undergo EMT acquire phenotypic changes, involving the upregulation and downregulation of molecules. The gene discussed is MICB; the disease is neoplasm.