A sarcopenic phenotype has been observed in transgenic mouse with neurotrypsin overexpression.26 In human plasma two stable and bio‐inactive circulating fragments of agrin—AgrinC110 (cleavage at α‐site) and CAF22 (cleavage at β‐site) were identified (Figure 1).21 It has been shown that elevated CAF22 plasma levels may indicate muscle wasting in pre‐frail community‐dwelling older adults because of degeneration of the NMJ.27 The reduction of CAF22 levels after 12 week power training supports CAF22 as a marker of muscle wasting and the development of sarcopenia. The gene discussed is AGRN; the disease is sarcopenia.