p21 responds to a variety of stimuli to promote growth-inhibitory activities that depend primarily on its ability to inhibit the kinase activity of cyclin-dependent kinase 2 (CDK2). p21-induced cell cycle arrest also depends on its ability to inhibit CDK1. p21 can inhibit cellular proliferation independent of CDK2 inhibition by inhibiting proliferating cell nuclear antigen (PCNA), which is required for S phase progression. Some of the anti-proliferative activities of p21 rely on its multiple protein–protein interactions and its ability to regulate gene transcription. The various physiological responses triggered by p21 are interconnected. For example, cell cycle arrest induced by p21 promotes DNA repair by allowing sufficient time for the damaged DNA to be repaired before it is passed to daughter cells and is a major route by which p21 exerts its anti-apoptotic activities. Similarly, the ability of p21 to regulate gene expression is important in promoting cellular senescence. The effect of p21 on gene transcription is generally inhibitory, but p21 can also activate gene transcription under certain conditions.

Article Abbas T, Dutta Ap21 in cancer: intricate networks and multip...

To finish Yoshida's answer, p21-kinases or PAKs are totally distinct from the p21Cip1 of cell cycle fame.  The p21 in one has nothing to do with the p21 in the other !

In PAKs (p21 activated kinases) the p21 refers to the ras gene family of GTPases that encode a group of related 21,000 dalton (p21) proteins.  These p21-proteins activate kinases called p21-activated kinases.  Thus, it is the coincidence of their molecular weights ! That's all.

See the attached papers and this abstract:  One of them is the original discover of PAKs

http://www.ncbi.nlm.nih.gov/pubmed/3333361