ACVR1B and Miyoshi myopathy: Notably, we found that the type I activin-A receptor ALK4 was selectively upregulated in the ALDHbright CICs in MM cells, and that the neutralization of activin-A and functional inactivation of ALK4 by shRNA or a low-molecular-weight inhibitor diminished the ALDHbright CIC population without affecting the spheroid formation of MM cells.