These molecules were shown to induce both cell cycle arrest of adult T-cell leukemia by decreasing cyclin D1 expression levels, and apoptosis by decreasing the expression levels of Bcl-xl and other anti-apoptotic factors [47, 48], but also to inhibit cancer cell proliferation, and suppress cap- or IRES-driven translation without affecting HCV IRES-mediated translation [49]. This evidence concerns the gene CCND1 and cancer.