As HF occurs, the downregulation of SERCA2a indicates that Ca2+ influx causes intracellular calcium overload, stimulating Ca2+ binding to CaMKII, leading to phosphorylation of the substrate of CaMKII, promoting its autophosphorylation, and the activated CaMKII directly phosphorylates CREB and binds with a specific sequence of cyclic adenosine phosphate response elements, recruiting RNA polymerase II, to form a transcription complex to control gene transcription [10, 11]. This evidence concerns the gene CREB1 and hydrops fetalis.