Within the mechanisms that could explain an upregulation of SALL2 expression in some cancers, it was recently shown that, similar to the binding of the large T protein of mouse polyomavirus to SALL2, the human papillomavirus type 16 E6 protein also interacts with SALL2 thereby stabilizing and increasing levels of a non-functional SALL2 protein [66]. Here, SALL2 is linked to cancer.