This suggests that with increasing obesity, the availability of vitamin K is reduced and hence gene expression levels are increased in an attempt to produce sufficient active VDKP and active vitamin K. Without excess vitamin K, over expression of Vkor increases the proportion of carboxylated to undercarboxylated VKDP as the rate of vitamin K hydroquinone production rather than the rate of vitamin K–dependent carboxylation can be the rate-limiting step for in vivo vitamin K–dependent protein carboxylation. The gene discussed is VKORC1; the disease is Obesity.