As speculated, knockdown of ZEB1 upregulated CDKN1A (P21CIP1) and CDKN2A (P16INK4A) (Fig. 6I and J), suggesting that both P16INK4A/RB1 and TP53/P21CIP1 tumor suppression pathways are deregulated with high expression of ZEB1 in UM cells leading to rapid cell proliferation with no risk of apoptotic cell death as downregulation of the above CDKIs would phosphorylate and inactivate RB1 so as to promote cell cycling9. This evidence concerns the gene ZEB1 and neoplasm.