In the current study, we used Atp2a2+/− mice on an inbred FVB/N background; while these heterozygous (HET) mice continued to display effects of SERCA2 haploinsufficiency in keratinized epithelia, cardiac performance was apparently normal, more closely reflecting findings in DD patients [6, 7]. The gene discussed is ATP2A2; the disease is dentin dysplasia.