In summary, based on the M-T-C interaction network, we found that RS-FZ treatment of HF may be due to the modulation of CYP2D6, EPHX2, MAOB, and ENPP2 by a variety of small molecules with potent cardiac, anti-inflammatory, anti-fibrotic and other pharmacological effects. This evidence concerns the gene CYP2D6 and hydrops fetalis.