These results showed significant 3’UTR shortening in HIV-1–infected cells compared with mock-infected cells, suggesting that HIV-1 infection induces 3’UTR shortening and the use of proximal polyadenylation sites, phenotypically resembling the APA patterns observed with the knockout (KO) of CFIm complex components, such as CPSF5 and CPSF6. This evidence concerns the gene CPSF6 and HIV-1 infection.