A vast number of enzymes are now known to derive their function from radicals that are produced by proton-coupled electron transfer (PCET), consequently placing this mechanism at the heart of radical enzymology. Of the enzymes that operate by PCET, ribonucleotide reductase (RNR) is exceptional in its biological function and is paramount to health as mis-regulation of RNR leads to disease states caused by imbalances in the intracellular deoxynucleotide pools available for replication and DNA repair, thus highlighting the enzyme’s potential as a therapeutic target. We now report that the turnover limiting step of the enzyme is the PCET transport of the radical from the cofactor to the interface.