To determine whether the phenomenon of supersaturation observed for IBM-associated proteins (Fig. 2b), an acquired PAM, is also observed for proteins associated with hereditary PAMs (hPAM), we extended our studies to proteomic datasets from laser microdissected myofibers of muscle biopsies of patients with three different genetically defined hPAMs (10 patients with DES mutations, 7 patients with FLNC mutations and 17 patients with MYOT mutations) [20, 25, 26]. The gene discussed is MYOT; the disease is inclusion body myositis.