Secondly, since we used systemic TNIP3 overexpression mice rather than cardiac-specific overexpression mice, we cannot rule out the possibility that TNIP3 and PI3K/Akt/NF-κB signalling in other cell types within the heart may contribute to the reduced susceptibility to VAs in the context of HF. Here, NFKB1 is linked to hydrops fetalis.