For Ankrd1, a member of the titin-N2A mechanosensory complex of the Z-disc30 with roles in muscle morphogenesis and remodeling, we find a strong downregulation, whereas an upregulation was observed in ALS muscle and after denervation23, 29 [noticeably, no Ankdr1 at all was detected in a study of central core disease (CCD) in humans, a disease linked to deficient function of RyR1 Ca2+ release31]. This evidence concerns the gene TTN and amyotrophic lateral sclerosis.