Current evidence indicates that MTs and related regulatory factors are involved in the resistance of cancer cells to ferroptosis.[163] Although direct evidence for MT regulating cuproptosis has not yet been obtained, it can be speculated that copper‐bound MT might function through a similar manner.[7a] Moreover, the activity of MT per se is modulated by GSH, and both are jointly governed by the NRF2 antioxidant signaling, thus linking cuproptosis with ferroptosis[7, 163] (Figure 7). The gene discussed is MCAT; the disease is cancer.