Interestingly, a loss of the Drosophila LRRK2 homolog also led to an activation of 4E-BP, acting to suppress Pinkl and Parkin pathology in these flies, suggesting that the pharmacological stimulation of 4E-BP activity may hold potential for PD therapy, especially in comparison to LRRK2, which has been traditionally difficult to selectively target without side effects. This evidence concerns the gene LRRK2 and Parkinson disease.