TENT5C and Miyoshi myopathy: Indeed, for both the tumor suppressor and antiviral functions of FAM46C, the relevant downstream phenotypes always come as indirect secondary effects: in MM, where there is high ER stress due to the highly secretory nature of plasma cells, unfolded proteins accumulate and autophagic dampening causes defective protein clearing, in turn causing apoptosis, while in HEK-293T cells, where autophagy is required for efficient viral replication, autophagic inhibition causes defective viral particle production.