TNFRSF12A and amyotrophic lateral sclerosis: Since the receptor has been proposed as the main effector of the TWEAK/Fn14 pathway activity [34] and that Fn14 can act independently from TWEAK in muscle [35], it is possible that manipulating Fn14 instead of TWEAK in the SOD1G93A ALS mice could lead to differential and/or improved benefits.