Digging up plots for a story of mine in late 2015, I came across paperwork upon paperwork, thesis and theories about body parts like limbs and appendages' regeneration. 

Something the Mexican Salamander does often.  

Yes! Some animals have the ability to regrow lost body parts at anytime, and by anytime, I mean at anytime and stage in their cycle. They can regrow parts like brain, spinal cord, limbs, and tails. 


Back to the human body, who's noticed we get injured and get healed, blood clots and the wounds get covered, but we don't regenerate lost body parts?


Taking my research off the edge, body part regeneration would be possible with the removal or absence of a gene(s).

Conclusion was drawn that it could be possible, like it does occur in the bodies of some reptiles that have the ability to regrow a lost tail, if the p21 gene was absent. 


The p21 gene naturally, is an anti-cancer gene among all its functions and if removed or reduced, would cause humans to be more prone to cancer, but enhance the growth or regeneration of lost body parts. Choosing cancer suppression over regeneration might not be put to work now. 


Tests have been carried out and the successful removal of the gene has worked on the lab mouse; ear holes tended to heal up without scars or display of previous injury, appendages regrew and all. If it worked on them, then it might work on us. Fear of cancer majorly, is just why no one smiling at this, but there might be a way around this. Scientists always have a way around their thing. They either find an alternative, or study some other animals that can regenerate and see why. Better still, any way can be worked around cancer suppression and all. The removal of the P21 gene might be tied to some other issues, but the main issue is that man would be more prone to cancer if the gene was removed.


P21. What it really means? 


As found on the net, the first definition might be a bit complex.


It is also known as CDKN1A


 A gene on chromosome 6p21.2 that encodes a cyclin-dependent kinase inhibitor, which binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, thus acting as a regulator of cell cycle progression at G1. CDKN1A expression is controlled by p53, a tumour suppressor that mediates p53-dependent cell cycle G1-phase arrest in response to various stress stimuli. CDKN1A is specifically cleaved by CASP3-like caspases, activating CDK2 and possibly also the apoptosis pathway.



 Also known as p53 protein, an anticancer protein of the class of cyclin-dependent kinase inhibitors. Cyclin-dependent kinases are enzymes that have been described by Elizabeth Finkel as ‘the engines that drive the cell-cycle past its various control checkpoints.’ Inhibition of these enzymes provides a way of controlling rapidly-reproducing cells such as cancer cells. High levels of p21 are found in ageing cells. p21 protein is dysfunctional in most human cancers.




©Godwin Okhuoya.