By combining microscale electrophoresis (MST) analysis and alpha-fold modelling, we demonstrated that the binding of the CRIB domain to Roc-COR is weakened by pathological substitutions at R1441 and Y1699 LRRK2 residues, which are both sitting at the binding interface, providing a rationale for the observed PD mutation-specific effect exerted by PAK6. Here, LRRK2 is linked to Parkinson disease.