p53 activation affecting other molecular pathways are being studied now...with the pill form of K, there's also the chance of bio-availability being increased multi-fold...aimho
In wild-type TP53 genes, p53 proteins are activated but inhibited by other proteins (MDM2, for example) so they can't function properly. Kevetrin can separate the p53-MDM2 complex so p53 can do its job.
In mutant TP53 genes, p53 proteins can't be activated by chance. Mutations in the DNA sequence produce the wrong p53 proteins every time. It's like an error in a computer program. It'll produce the wrong result every time unless the error is fixed. Kevetrin can degrade mutant p53 so they can't promote tumor growth.
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