found that IL-34 deficiency repressed both the canonical and non-canonical NF-κB signaling pathway, leading to a marked reduction in P-IKKβ and P-IκBα kinase levels and the downregulation of NF-κB p65, RelB, and p52 expression, which drove the decline in chemokine CCL2 expression, thus alleviating cardiac remodeling and HF post-ischemia/reperfusion (19, 20). This evidence concerns the gene IL34 and hydrops fetalis.