The capability of FAM46C to stabilize specific transcripts, and hence favour their expression, was later confirmed by others both in MM [30,66] and outside the tumoural environment, specifically in plasma cells [30], terminally differentiated B cells [71] and osteoblasts [17], making the poly(A) polymerase model the one most widely accepted to explain a mechanistic role of FAM46C. Here, TENT5C is linked to Miyoshi myopathy.