Kim1 triggers efferocytosis of apoptotic cells by PTECs (24, 25), while loss-of-function studies using Havcr1 mutant mice show that loss of Kim1 expression or PS binding function exacerbates ATI, increases tubular cell apoptosis and necrosis, and increases inflammation after AKI (26–28). This evidence concerns the gene HAVCR1 and acute kidney injury.