PLCβ1 is a direct target for miRNA106a, while the NF‐κB pathway is indirectly targeted by decreased Camk2δ (an miRNA106a target) signalling to IκBα.[48, 49] This two‐pronged, in vitro/in vivo approach establishes a thorough feasibility outcome/proof‐of‐concept for CTP‐miRNA106a mechanisms and its ability to reverse HF parameters in mice. The gene discussed is NFKBIA; the disease is hydrops fetalis.