Tsa1 may influence mutation rates in a direct and/or an indirect way. Given the three biochemical activities of Tsa1 and related peroxiredoxins (i.e., peroxide detoxification, molecular chaperone activity, and redox switch activity), it is possible that any of these directly contribute to suppressing mutations. However, there is evidence suggesting that Tsa1 may influence genomic stability by titrating thioredoxin away from other substrates involved in DNA synthesis or repair, most notably ribonucleotide reductase. In the case of the Tsa1-ribonucleotide reductase competition hypothesis, Tsa1-mediated thioredoxin (Trx) sequestration may be a way of regulating ribonucleotide reductase activity, thereby maintaining appropriate dNTP levels and lowering mutation rates.