CASP8 and hydrops fetalis: During cardiac contraction, the p38 pathway promotes the release of Ca2+ from the sarcoplasmic reticulum.49 Considering that the overload of Ca2+ can lead to cell death and that RIPK1, caspase 8 and Fas-associated protein (FADD) can interact to form the RIPK1-FADD-caspase 8 complex, causing pathological cardiac remodeling and HF by inducing necrotic cell death,51,52 we examined the effect of 2-APQC on this signaling pathway.