signaling of GHSR‐1a possibly due to the receptors translocation from the membrane to the nucleus (Leung et al. 2007). The rs2948694 SNP, although located in a non‐coding region of either GHSR transcripts, could tentatively affect the splicing of the gene and cause a shift in GHSR‐1a and GHSR‐1b transcription, however, this remains to be confirmed. Furthermore, the SNP is in close proximity to a previously studied two‐base pair deletion (Gueorguiev et al. 2009), rs10618418, and although we were not able to find any data on the linkage disequilibrium (LD) between these two SNPs, the previous study report strikingly similar genotype frequencies as seen for rs2948694 in the present study. It is thus possible that the markers are in strong LD and it is rather the effect of the deletion that is being studied here. Nevertheless, the functional value of this deletion remains to be determined.
