To date, more than 18 genomic intervals, which underpin the complex myriad of extracellular matrix interactions of tendons, have been implicated in risk models for tendinopathy. It is these relationships that most likely regulate the tissue's response to loading and unloading, thereby dictating the overall capacity of tendons and influencing injury susceptibility. The evidence suggesting a genetic contribution to the susceptibility of sustaining a tendon injury is growing. However, only a few of the loci have been repeated in independent studies, of which some have included a range of musculoskeletal soft tissues injuries. Case-control study designs can be effective in capturing risk, provided that the cases and controls are equally well-defined and carefully considered. The genome consists of 3.6 × 10(9) sequences and therefore we realise that we are far from decoding all the genomic signatures. We are indeed fortunate to be living in such exciting times where high-throughput technologies are at our disposal. Through collaboration, our chances of harnessing these "omics" technologies to further our clinical understanding of tendinopathy will increase.