This also means that adequate mitochondrial trafficking and supply is critical not only in the case of motoneuron terminals, but to intrafusal proprioceptive terminals as well under unaccustomed or strenuous eccentric contractions, otherwise it is proposed to lead to TAD-like lesions or, more precisely, to Piezo2 channelopathy [8,12]. This evidence concerns the gene PIEZO2 and channelopathy.