Romain and coworkers identified that both PCAF and CXCL12 were downregulated in colorectal tumor samples and found that a PCAF expression plasmid could significantly increase the CXCL12 gene expression level, which drove them to speculate that acetylation of the CXCL12 promoter may explain this phenomenon[36]. This evidence concerns the gene KAT2B and colorectal neoplasm.