Other Ca2+ channels, which we observed to be up-regulated in AKI, and that could potentially contribute to Ca2+-overload are Ca2+-import channels such as voltage-sensitive calcium channels VSCC (isoforms Cacna1g/h and Cacnb1) and transient receptor potential channels TRP (isoforms Trpc4, Trpm1/3), intracellular release channels sarcoplasmic/endoplasmic reticulum calcium ATPases SRCA (isoforms Atp2a1/2) which are dependent on ATP hydrolysis, and others (Slc8a3, Ryr1). The gene discussed is ATP2A1; the disease is acute kidney injury.