Moreover, since p27Kip1 can also be regulated by p53-dependent ubiquitin ligases18 but its depletion alone is unable to enhance basal cell proliferation in p53-mutated FN-RMS cells with intact SKP2 expression, our data suggest that SKP2 is the primary factor maintaining p27Kip1 protein levels under a functional threshold in our tumor model. This evidence concerns the gene SKP2 and neoplasm.