HDAC3 inhibitor treatment increases the Ac-H3 level at B7x promoter and promotes the interaction of C/EBP-α with the B7x promoter to upregulate the expression of B7x, an immune checkpoint molecule crucial to the immune escape of tumors, which contributes to HDAC inhibitor resistance in CRC[44]. This evidence concerns the gene VTCN1 and colorectal carcinoma.