Regions of low oxygen (hypoxia) occur in most solid tumours and correlate with poor patient prognosis. Importantly, hypoxia also leads to resistance to radiotherapy. Previous work from my lab has described the DNA damage response which is initiated in response to hypoxia-induced replication stress. The cause and consequence of this replication stress is the subject of on-going work in the lab. Currently, we are focused on the ribonucleotide reductase (RNR) enzyme, which is an oxygen-dependent enzyme that is responsible for the de novo conversion of NDPs to dNDPs – the building blocks of DNA synthesis. One of the small subunits of RNR (RRM2B) has been shown previously to be induced after DNA damage and specifically after irradiation. The purpose of our study was to investigate if RRM2B has a role for maintaining replication in hypoxic conditions (<0.1% O2), these data will be discussed.