RPL10 and neoplasm: However, SOX9 overexpression enabled these tumor cells to evade immune surveillance, possibly by upregulating inhibitory ligands such as UL16-binding proteins (ULBPs), Which a novel MHC class I-related molecules, bind to CMV glycoprotein UL16 and stimulate NK cytotoxicity through the NKG2D receptor (Malladi et al., 2016), This suggests that SOX9 may play a crucial role in helping tumor cells escape NK cell-mediated killing.