In some cases, the nature of the interaction of the gene products in a triallelic digenic inheritance pattern can be deduced—for example, in the case of cortisone reductase deficiency (MIM #604931) due to an intronic mutation in HSD11B1 (MIM *600713.0001) and exonic mutations in H6PD (MIM *138090.0001 –*138090.0002).68 The long QT syndromes, in which the interaction of mutations in two different ion-channel genes appear to occur, provide other examples. OMIM records two examples of the LQT syndrome resulting from double heterozygosity for mutations in two LQT genes—that is, biallelic digenic inheritance. LQT 1/2 results from heterozygous mutations in the KCNQ1 (MIM *607542.0009) and KCNH2 (MIM +152427.0019) genes, and LQT3/6 results from heterozygous mutations in the SCN5A (MIM +600163.0007) and KCNE2 (MIM +603796.0005) genes. LQT 2/5 can result from a heterozygous mutation in the KCNH2 (MIM +152427.0021) gene and a homozygous mutation in the KCNE1 (MIM *176261.0005) gene, another example of triallelic digenic inheritance.