High cytosolic calcium input in HF is particularly attributed to the dysfunction of the L-type calcium channel (LTCC); indeed, increased phosphorylation of LTCC is evident in HF and results in a compensatory leak of sarcoplasmic reticulum (SR) calcium through ryanodine receptor 2 (RyR2), which is in the uncoupled form due to chronic SNS stimulation and oxidative stress [27,28]. This evidence concerns the gene RYR2 and hydrops fetalis.