In most MM patients, cPC produce a clonal immunoglobulin—Ig (i.e., M-component)—which becomes detectable in blood and/or urine, in association with decreased normal residual serum Igs levels (i.e., immunoparesis) and end-organ damage (e.g., cytopenia, anemia, lytic bone lesions, renal failure) [3,4]. Here, CUBN is linked to Miyoshi myopathy.