The statistical power was slightly lower to identify similar effect sizes for PHV in infancy and puberty, and even lower to identify age-SNP interactions. Despite this, we found an interaction with a p-value of 0.0030 that together with a meaningful biological explanation gives suggestive evidence for a differential SNP effect by age. This SNP lies in SOCS2 (Suppressors of cytokine signalling 2) which is a negative regulator of cytokine and cytokine hormone signalling via JAK/STAT pathways, and one of its functions is to influence growth and development through effects on growth hormone/IGF-1 signalling [19]. Estrogen has been shown to induce SOCS2 expression in vitro, with a subsequent decrease in JAK-STAT signalling in response to growth hormone [20]. This potential role for SOCS2 in the interplay between steroid hormones and growth, could explain the association we observe between SOCS2 variation and growth velocity during puberty. The lack of association in early infancy could be explained by the fact that height growth is not yet dependent on growth hormone at that age [14]. Also, we found a possible biological explanation for the
