These mechanisms generally serve to adapt to proteotoxic stress via expansion of the proteosynthetic apparatus, e.g., via stabilization of terminal nucleotidyltransferase 5C (TENT5C), also known as FAM46C, a non-canonical poly(A) polymerase, which boosts ER growth in MM and which is tightly regulated via proteasomal degradation and autophagy (259). Here, TENT5C is linked to Miyoshi myopathy.