ATP7B and Wilson disease: The differences between the high level of carriage of the pathogenic variants of the ATP7B gene and the low registration of WD can be explained both by underdiagnosis, by the level of genetic research methods, and by the lack of agreement among geneticists in a unified approach to the analysis of the data obtained, since there is already evidence that the clinical manifestations of WD depend not only on the sensitivity of tissues to copper toxicity, but on the location and type of pathogenic variant of the ATP7B gene [84].