For Cu trafficking, the negative regulatory factor of cuproptosis MTF1 is capable of binding to the metal-responsive element of ATP7B promoter, their failed interaction may contribute to the unusual Cu efflux in Wilson disease (Stalke et al., 2020); for Cu reservation, MTF1 can bind to the metal-responsive element in the upstream of metallothionein and the elevation of metallothionein reduces the intracellular free Cu ions in response to Cu stress (Adams et al., 2015). This evidence concerns the gene MTF1 and Wilson disease.