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