A classical myomiR, miR-133a is predicted to target TUBA4A, which was recently shown to be involved in ALS66,67, and has also been shown to change during myogenesis68, in response to physical activity69,70, aging71 as well as during neuromuscular regeneration and reinnervation in a rat denervation model72, and has recently been shown to be increased in early-stage and slow-progressing ALS patients34. The gene discussed is TUBA4A; the disease is amyotrophic lateral sclerosis.