For example, SAM68 is able to promote the production of the oncoprotein E6 of the human papilloma virus (HPV) type 16 [123], which is a known etiological agent for human cervical cancer [124]. E6 alternative splicing is controlled by EGF through activation of ERK1/2-kinase that promotes SAM68 phosphorylation, suggesting a possible implication of SAM68 in HPV E6 splicing during differentiation and the viral life cycle processes of cervical cancer. This evidence concerns the gene EGF and cervical cancer.