Tricostatin A (TSA) is a protein deacetylase inhibitor. You know that HDACs remove acetyl groups from lysines. You are interested in identifying how TSA works. You do a number of experiments. You find the level of a protein, called survivin is increased 10-fold in cells when you treat with TSA. You assume this is at the level of transcription. You measure the mRNA for survivin and find it is unchanged. Can you think why TSA increased survivin protein?