Based on our in vitro and in vivo data, we believe CTP‐miRNA106a could address an unmet medical need for delivery of a molecular therapeutic to treat HF that goes directly to cardiomyocytes and acts on HF hub signalling pathways such as CAMKIIδ, PLCβ1, and NF‐κB pathways. This evidence concerns the gene NFKB1 and hydrops fetalis.