If NNAT functions as an inhibitor of SERCA2 so that silencing or upregulation of NNAT expression results in transient or sustained changes in [Ca2+]i, then the phenotype resulting from NNAT silencing may be variable among tumor types dependent upon the dynamics of the Ca2+i response, the lineage-specific or differentiation stage-specific portfolio of calcium-responsive genes and proteins, and/or the cell sensitivity to ER stress responses including apoptosis resulting from perturbation of Ca2+i homeostasis. This evidence concerns the gene ATP2A2 and neoplasm.