However, despite the induction of MYH2/MyHC expression and enhancement of MyHC positive p57Kip2-overexpressing tumor cells, the extent of differentiation was modest with respect to that shown by SKP2-depleted cells (Supplementary Fig. 7c–e), suggesting that SKP2 silencing provides a pro-differentiation cell context in which p57Kip2 highly support the myogenic program. This evidence concerns the gene CDKN1C and neoplasm.