Preceding the development of tau pathology, changes in actin-dependent processes, including the formation of rods and mis-localization of Drp1, have been observed in neurons in different neurodegenerative disease models [224,267,312,332,333], suggesting that the sequestering of cofilin into cofilin-actin rods could be contributing to defects in many other diseases. The gene discussed is CFL1; the disease is neurodegenerative disease.