In addition, it is often the case that drug selectivity for a pathogen arises due to idiosyncrasies in pathogen physiology such as slower turnover of the target protein allowing for more pronounced drug action, e.g., ornithine decarboxylase in Trypanosoma brucei, the causative agent of African Sleeping Sickness [40], differences in protein regulation, e.g., dihydrofolate reductase in Plasmodium falciparum[41] or a lack of functional redundancy compared to the host [42]. The gene discussed is ODC1; the disease is human African trypanosomiasis.