Interestingly, the carcinogen arsenite could transcriptionally induce MALAT1 via HIF2α, and MALAT1 was found upregulated in the sera of people exposed to arsenite as well as in HCC patients; in turn, MALAT1 was able to promote the disassociation of the von Hippel-Lindau (VHL) protein from HIF-2α, therefore alleviating VHL-mediated HIF-2α ubiquitination and degradation. Here, VHL is linked to hepatocellular carcinoma.