These results are more consistent with a Fetal Insulin Hypothesis model of the relationship between birthweight and cardiometabolic disease, which posits that the same genetic factors that alter intrauterine growth also affect future risk of disease [14] (i.e. diabetes risk alleles in the mother result in higher levels of circulating glucose tending to increase offspring birthweight, whereas many of the same loci in the fetus decrease sensitivity to insulin, tending to decrease offspring birthweight, and predisposing the child to T2D in later life), than a Barker type model. The gene discussed is INS; the disease is diabetes mellitus.