Whether this T3 effect is driven solely or partially by T3 upregulation of Jph2 is unclear, but data from animal studies either overexpressing Jph2 or reexpressing Jph2 in heart failure models support Jph2’s role in promoting ion channel organization, possibly driven by direct physical interactions of Jph2 with both RyR2 and LTCC (27, 28, 46). The gene discussed is JPH2; the disease is heart failure.