Such aberrations are likely to assist tumor progression, as deficient p21 is unable to prevent cell cycle progression and DNA synthesis through cyclin-CDK complexes or PCNA inhibition [228,229,230,231,232], while in the case of M38Nfs*10 frameshift insertion, the intact 33 NH2-terminal aa residues, where procaspase-3 binding domain is located, might further facilitate tumor progression due to sustenance of p21 anti-apoptotic activity [233,234]. Here, CDKN1A is linked to neoplasm.