Therefore, we presented the following questions based on the above-mentioned observations: 1) miR-145 may acts as a crucial regulator in CaMKII signaling pathway for determining cardiac remodeling after HF; 2) whether miR-145-induced depression on CaMKII might compensatorily promote βAR-Gs-PKA cascades, since both CaMKII and PKA activities are both required for the modulation of ICa channels and intracellular contractile myofilaments. The gene discussed is ADRB2; the disease is hydrops fetalis.