The complex transcriptional and post-translational modification of the NFKB1 gene and product, respectively, might be the reason why the several studies addressing ablation of the NFKB1 gene present different conclusions: sometimes observing that NFκB (p50) acts worsening HF by activation of a pro-inflammatory pathway[13-16] whereas in other, protecting the heart by activation of anti-inflammatory pathways, matrix remodeling or attenuation of oxidative stress[19]. This evidence concerns the gene NFKB1 and hydrops fetalis.