Genome-wide association studies have transformed our understanding of the pathophysiology of common diseases in the last 15 years, and risk prediction through polygenic risk scores is now a reality. For myopia, the first two common genetic variants were described in 2010, and within ten years almost 450 genetic loci were identified, with the power obtained through increasingly large studies, the most recent including over half a million participants. Refractive error, and myopia in particular, is not dissimilar to height genetically, in that the trait is highly heritable but that risk is transmitted through many risk variants all of relatively small effect size. In keeping with our understanding of the physiology of emmetropisation being driven by the retina sensing defocus and regulating eye growth, stimulating axial elongation where there is hyperopic defocus and stopping growth when emmetropia or myopia is reached, many genes involved in retinal signalling have been associated with myopia. Where mutations in genes cause often devastating retinal dysfunction and impair vision, the common variants identified may cause (or are markers of) relatively minor functional changes, resulting in disturbance of the normal physiological processes. In common with many other GWAS studies, there is still a limited knowledge of the mechanisms involved. One of the commonest risk variants of strongest effect is on chromosome 15, near the GJD2 gene which encodes the Connexin-36 protein, forming retinal gap junctions. Other examples include KCNQ5, GRIA4, CACNA1D, RGR, RDH5, GNB3 and RORB.  Bioinformatic tools (eg DEPICT) show the most significant gene sets associated with myopia are ‘abnormal photoreceptor inner segment morphology’, ‘thin retinal outer nuclear layer’, ‘detection of light stimulus’ and ‘nonmotile primary cilium’. Other genes that appear related to refractive error include those associated with circadian rhythm and pigmentation.