But unlike in cancer cells where MALAT1 binding facilitates PRC2 to be associated with the promoter of specific gene locus (53–55), in HIV infection, the binding of MALAT1 with PRC2 displaced its catalytic component EZH2 from binding to HIV-1 LTR promoter, and thus preventing the HIV-1 LTR from PRC2-mediated epigenetic silencing. This evidence concerns the gene MALAT1 and HIV infectious disease.