Since the aforementioned markers correlated, not only at a cell population level, but also at a single cell level as seen from serial sections, as opposed to the main tumor mass which displayed inverse levels [127], it has been suggested that the p16INK4 increase sequesters Cdk4 in the cytosol, thus enabling nuclear cyclin D1 to bind Cdk2, which competes with (and prevents) binding of cyclins A and E to Cdk2, resulting in the decreased proliferation reported in tumor buds [128]. This evidence concerns the gene CDKN2A and neoplasm.