AQP4 and neuromyelitis optica: Cuproptosis can cause differences in cell death through the tricarboxylic acid (TCA) circle.[7, 8] Interestingly, the TCA cycle is crucial for the differentiation of naïve T cells,[9] including the polarization of regulatory T cells (Tregs)[9] and T helper 1 cells (Th1) et al.[10] While pathogenic B‐cell‐derived AQP4‐IgG remains the primary effector mechanism in neuromyelitis optica spectrum disorder (NMOSD), emerging evidence indicates that NMOSD pathogenesis involves dysregulated crosstalk between humoral and cellular immunity—not merely humoral dysfunction.