Abstract
Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E(2) (PGE(2))/protein kinase A (PKA)-mediated inactivation of the pro-apoptotic protein BAD. However, the PGE(2)/PKA pathway is not the only means to inactivate BAD and limit cell death. This Commentary shows a broader picture of this pathway to examine the kidney's BAD options.