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Since the loss of high-affinity drug binding was always correlated with a loss of C-type inactivation, it is possible that the changes observed in drug binding are due to indirect allosteric modifications in the structure of the channel protein and not to the direct interaction of dofetilide with the respective mutated site chains

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If absorption corrects, this favors the deficiency of the endogenous intrinsic factor as seen in pernicious anemia