In basal conditions, AMBRA1 is maintained in an inactive state by mTOR phosphorylation and by its anchoring to the dynein motor complex. After autophagy induction, AMBRA1 and ULK1 are active; AMBRA1 enhances ULK1 kinase activity and stability by promoting its Lys-63-linked ubiquitylation and self-association through TRAF6. ULK1 primes AMBRA1 detachment from the dynein complex through a positive phosphorylation. Coupling these regulatory events may represent a positive feedback to sustain autophagy in a continuous loop. The exocyst may act as a scaffold platform to keep the complexes involved grouped together. 