Autophagy is a key cellular process that degrades unwanted, damaged or toxic cellular intracellular components and its dysfunction has been linked to many diseases ranging from cancer to neurodegeneration. The kinase ULK1 is critical in initiating autophagy and is thus an attractive therapeutic target, yet we do not fully understand how ULK1 controls autophagy induction. Using ULK1 inhibitors developed by the Ganley Lab and others, former PhD student Maria Zachari and current student Marianna Longo were able to show that ULK1 inhibition blocks autophagy but in an unexpected way. Using these structurally distinct inhibitors they unexpectedly found that autophagic structures still formed but they did not mature and traffic to lysosomes. While this works highlights that pharmacologically targeting ULK1 is a therapeutic way to block autophagy, it also shows that ULK1 kinase activity plays a critical role in the maturation of autophagosomes and not just in initiating their formation. These finding have just been published in Life Science Alliance and can be accessed here.