SOAT1 and acute kidney injury: Our model suggests a cascade of signaling events involving up-regulation of canonical- and down-regulation of non-canonical- Wnt signaling that may result in decreased intracellular Ca2+ concentration, resulting in an increase of intracellular cAMP levels that in turn stimulates MAPK/ERK signaling leading to proliferation, followed by increased Jak-STAT signaling and inflammation (Figure 10), ultimately leading to renal failure.