Interestingly, similar to TDP-43, frameshift mutations in the PrLDs of HNRNPA2B1 and HNRNPA1 that change the prion-like behaviour of the mutant proteins have been described recently as the genetic cause of myopathies [6, 29], whereas most of the missense variants in the exact same protein domain can be linked to a broader clinical spectrum including neurodegeneration [7, 28]. Here, HNRNPA1 is linked to myopathy.