Because of the shift to proximal poly(A) sites that correlated with mRNA up-regulation, described in the OPMD mouse model [20], we asked whether a similar mechanism could lead to increased Smg levels in Drosophila muscles expressing PABPN1-17ala and underlie increased deadenylation. The gene discussed is SAMD4A; the disease is oculopharyngeal muscular dystrophy.