Factors determining the responsiveness to antithyroid drugs (ATDs) in Graves' disease are not fully known. Notwithstanding the typical pattern and tempo of thyroid hormone responses to thionamides, the existence of an unusual subset of Graves' disease with extraordinarily rapid thyroid hormone responses to ATDs will prove challenging even to the expert clinician. Termed 'rapid responder Graves' disease' or 'high turnover Graves' disease', the serum thyroxine (FT4) and triiodothyronine (FT3) of patients with this variant of thyrotoxicosis can decline precipitously during the initiation of ATDs and yet escalate acutely upon discontinuation of pharmacological intervention. We describe a case that presented with low serum FT4 and FT3 in association with suppressed serum thyrotropin (TSH) concentrations soon after starting carbimazole even at a low dose. The erratic clinical course comprising largely of serum FT4 nadirs and peaks is elaborated to facilitate appreciation of the difficulty in the stabilization of the thyroid with ATDs. The possible pathogenetic mechanisms for the chaotic fluctuations in thyroid hormones to minor changes in thionamide dose adjustments are discussed as well.