Since the first demonstration that rodent muscles could be genetically modified to increase strength (Barton-Davis et al., 1998) and subsequent publications showing that muscles may also be genetically modified to improve endurance, there has been substantial interest in the potential for a genetic approach to doping. In 2004 gene doping was included in the WADA prohibited list with the following definition: ‘‘Gene or cell doping is defined as the non-therapeutic use of genes, genetic elements and/or cells that have the capacity to enhance athletic performance”. Based on animal studies, a wide range of potentially athletically advantageous genes can be transferred into target cells using a gene vector. Genes that have been shown to enhance athletic performance in rodents with increased expression include insulin-like growth factor 1, erythropoietin, peroxisome-proliferator-activated receptor (PPAR) delta, PPAR gamma co-activator alpha or beta and phosphoenolpyruvate carboxykinase. Down regulation of myostatin activity has also been demonstrated to increase muscle mass. It should be noted that many of the genetic effects were observed in transgenic mice that inherited the genetic modification in the germline and thus developed in the presence of the difference in gene expression whereas the potential application for gene doping would be through the modification of somatic tissues in juvenile or adult humans. The likelihood of gene doping is enhanced by the research into gene therapy for muscle diseases such as Duchenne muscular dystrophy. The current method of choice for gene therapy in the clinical setting is through the use of adeno-associated viral (AAV) vectors carrying the therapeutic gene and these have been shown to be very effective in animal models of various muscular dystrophies but to date use in man has been limited to local delivery to single muscles. We are likely to see systemic delivery of AAV in human clinical trials for a number of neuromuscular diseases over the next few years which, if successful, could increase the possibility of athletes using gene therapy techniques. However, one significant limitation to potential gene dopers is that it is very technically demanding to produce the quantity of AAV required for high efficiency gene delivery to teenage or adult humans due to the large mass of muscle. A new and emerging area of concern relates to gene editing. A number of systems have been developed to allow researchers to make precise modifications to the genome and these are being refined rapidly. All of these methods involve some system for targeting specific genetic sequences couple to a nuclease that cleaves the genomic DNA. Methods developed to date include the zinc-finger nucleases, TAL effector nucleases (TALENs) and CRISPR/Cas9. The latter system developed rapidly in 2015 and has been used to modify the genome when delivered systemically using an AAV viral vector (Nelson et al., 2015). To the best of our knowledge gene doping has yet to be used by athletes. This is likely due to the current technical hurdles that prevent high efficiency gene delivery to muscle. There have also been a number of pro-active studies to identify methods for detecting gene doping that have shown potential to catch cheating athletes. Finally like many other forms of doping there are significant health risks and unlike conventional pharmaceuticals an athlete cannot stop taking the treatment if they have undergone genetic modification which increases the level of risk.