Thus, we postulate that the CaMKIIδB-induced NCX1 up-regulation is transcriptionally mediated in the TAC model, which may include the translocation of HDACs to the cytosol and MEF2 transcripts, as well as lead to increased expression of proteins directly involved in compensatory Ca2+ homeostasis. The gene discussed is SLC8A1; the disease is persistent truncus arteriosus.