PAX2 and acute kidney injury: Indeed, our data demonstrate that: (1) AKI involves a permanent loss of TECs even when GFR recovery occurs; (2) Pax2+ TECs are endowed with higher resistance to death and clonogenic capacity and are responsible for both spontaneous and drug-enhanced regeneration of necrotic tubule segments after AKI; (3) Only Pax2+ TECs complete mitosis, while other TECs rather undergo endoreplication-mediated hypertrophy; (4) Endocycle is a dominant TEC response upon AKI also in humans.