A disturbed Ca2+ homeostasis in cardiomyocytes of CKD mice could also be improved by blocking the proinflammatory innate immune receptor NOD1 (nucleotide-binding oligomerization domain-containing protein 1) or its downstream kinase RIP2 (receptor-interacting serine/threonine protein kinase 2).154. This evidence concerns the gene RIPK2 and chronic kidney disease.