Recent studies have shown that GDF-15 secreted by M2-polarized tumor-associated macrophages promotes ferroptosis resistance in AML cells by modulating the SLC7A11/GPX4 axis (Lu and Liao, 2025); however, this mechanism has not yet been validated in MM, and the roles of other immune cells within the TME remain unexplored. This evidence concerns the gene SLC7A11 and Miyoshi myopathy.