In this work, we report actin binding and bundling functions for YARS1, and demonstrate that they are relevant for CMT pathogenesis, as genetic manipulations of the actin cytoskeleton rescue cellular hallmarks of the neuropathy in Drosophila. Furthermore, we demonstrate that F-actin binding is a common feature for other disease-implicated synthetases and its manipulation can be beneficial for GARS1 neuropathy. The gene discussed is GARS1; the disease is neuropathy.