Considering that VprBP kinase activity toward H2AT120 plays a causal role in tumorigenesis, we also have developed a small-molecule inhibitor, named B32B3, capable of targeting VprBP catalytic domain, attenuating H2AT120p, and blocking tumor growth, even causing some partial tumor regression, in colon and prostate cancer xenograft models [7, 8]. This evidence concerns the gene DCAF1 and neoplasm.