In addition, the cross-bridge cycling kinetics (ktr) were significantly lower in HF compared to the donor, which is indicative of the slowing of actin–myosin turnover at saturating [Ca2+], and this was reversible upon treatment with GSH, but no effect was observed after PKA and/or PKC treatment (Figure 1C,G,K). The gene discussed is PRRT2; the disease is hydrops fetalis.