EXOC5 and acute kidney injury: Furthermore, a study in renal tubular MDCK cells showed that the mechanism by which the overexpression of exocyst Sec10, which is a highly conserved eight-protein complex that regulates protein trafficking, increases phosphorylation of ERK and healing from oxidative injury is EGFR, MAPK, and endocytosis dependent (Fogelgren et al., 2014), thereby highlighting the potential use of exocyst Sec10 as a therapeutic target in AKI therapy.