For instance, OPTN silencing delayed muscle regeneration in mice and impaired myogenic differentiation in C2C12 mouse myoblasts [72], and RNA-binding proteins whose mutations cause ALS, such as hnRNPA1, hnRNPA2B1, or MATR3, control myogenic cell fate transitions during differentiation by regulating the expression and alternative splicing of muscle-related genes [2, 32, 50, 83]. Here, OPTN is linked to amyotrophic lateral sclerosis.