Park and colleagues showed that the overexpression of SERCA2 and Bcl-2 is a consequence of the repositioning of the nuclear factor kappa B (NF-kB) secondary to calcium/calmodulin-dependent protein kinase 2 alpha (CaMK2α) activation in metabolic stress-resistant breast cancer cell lines MDA-MB-231 and MCF-7 [82, 83]. The gene discussed is NFKB1; the disease is breast cancer.