LRRK 2 directing ER ‐to‐ G olgi transport? ( ER )y ES !

Mutations in leucine‐rich repeat kinase 2 ( LRRK 2) represent the most frequent genetic lesions associated with Parkinson's disease ( PD ). LRRK 2 function and the pathogenic mechanisms of LRRK 2 genetic mutations remain poorly understood. Cho et al report in this issue of The EMBO Journal a new interaction between LRRK 2 and the ER exit site ( ERES ) protein Sec16A, important for anterograde transport of secretory proteins. Moreover, a disease‐associated mutation disrupts LRRK 2–Sec16A interaction and ERES function.