B2M and neoplasm: On the contrary, the Kobayashi team utilized a gene-specific system based on CRISPR/Cas9 technology, designated as TRED-I (Targeted reactivation and demethylation for MHC-I), to accomplish targeted demethylation of the NLRC5 promoter, induce an augmentation in NLRC5 expression, thereby upregulating MHC-I, B2M, TAP1 and genes encoding immune proteasome components (LMP2/PSMB9/β1i, LMP7/PSMB8/β5i), ultimately culminating in enhanced tumor immunogenicity (37).