Furthermore, CD36 facilitated CD8 + T lipid peroxidation and ferroptosis through the absorption of FAs enriched in BMM of MM, culminating in CD8 + T effector function impairment, while arachidonic acid (AA) emerged as the principal FA in BMM, triggering ferroptosis in CD8 + T [28]. The gene discussed is CD8A; the disease is Miyoshi myopathy.