[10] Likewise, miR-106a∼363 and its paralogs have been shown to promote proliferation of cultured cells by targeting p21Cip1/Waf1 and p63. [32], [33] Thus it is somewhat surprising that our gene expression observations suggest that, in terms of its interaction with Xpcl1, the effect of p27Kip1 loss is to overcome an anti-tumor activity of Xpcl1, as opposed to enhancing Xpcl1's oncogenic effect. This evidence concerns the gene CDKN1A and neoplasm.