Our key findings were: (1) vitamin D deficiency as determined by 25-hydroxy vitamin D levels in healthy humans were associated only with a suppression of resting overall cardiosympathovagal balance; and (2) lower levels of 1,25-dihydroxy vitamin D, the activated form of vitamin D, were associated with unfavourable shifts in cardiosympathovagal balance, driven by exaggerated withdrawal of cardioprotective vagal tone, in response to AngII challenge. The gene discussed is AGT; the disease is vitamin D deficiency.