Wilson disease (WO) is a treatable monogenic autosomal disorder present from birth but clinically manifested after copper overload at the median age of 10 to 23 years. Copper is one of the nutritionally essential micronutrients as it forms cofactor to a large number of regulatory enzymes active in normal metabolism. If copper  trafficking  is defective.  intracellular levels of copper start rising, which causes disturbances in structure and function of cuproenzymes and can generate superoxide radicals. Above certain levels of intracellular copper accumulation, it could even enter the nucleus and damage DNA causing unpredictable damage to the cellular functions. The gene associated with WO has been identified in last two decades as atp7b. Bioinformatics Applications are made to understand molecular genetic causes of the WO and to design a DNA chip for early and accurate detection of WD mutants in clinically complex patients.