MALAT1 is expressed at high levels in HIV-infected cells, where it enhances HIV transcription from latent provirus [78]; it localizes EZH2 to its target sites in tumors; and in HIV infection, it sequesters EZH2 away from the HIV long terminal repeat (LTR), thus preventing PRC2-mediated H3K27 trimethylation and promoting HIV viral reactivation [78]. This evidence concerns the gene EZH2 and HIV infectious disease.