FKBP1A and hydrops fetalis: We saw that aldosterone, a neurohormone involved in HF, (1) activates LTCC expression (Bénitah and Vassort, 1999), (2) increases diastolic Ca2+ release by decreasing the expression of the RyR accessory proteins FKBP12 and 12.6 (Gomez et al., 2009), and (3) decreases the expression of the channel responsible for the transient outward potassium current (Ito) secondarily to an increase in [Ca2+]i and activation of Cn (Bénitah et al., 2003; Perrier et al., 2004), thereby recapitulating some of the outcomes of HF (Bénitah et al., 1993, 2002; Gómez et al., 1997; Marx et al., 2000).