Indeed, many top marker genes were previously reported to be mutated in human myopathies (Flnc, Klhl40, and Fhl1)40–42 or to directly interact with proteins whose mutation causes disease (Ahnak interacts with dysferlin; Hsp7b or Xirp1 interact with Flnc)43–45. This evidence concerns the gene KLHL40 and myopathy.