In contrast to the early embryonic lethality of homozygous mutant Ap2s1 mice (Ap2s1del17/del17), heterozygous mutant Ap2s1 mice (Ap2s1+/del17) were viable and appeared normal, and this is similar to the findings in heterozygous Ap2μ+/− and Ap2β+/− mice.39, 43 However, the Ap2s1+/del17 did not have the plasma and urine biochemical abnormalities associated with FHH3, and these included an absence of hypercalcemia and hypocalciuria (Fig. 6, Tables 1 and 2). This evidence concerns the gene TFAP2B and Hypercalcemia.