We read the recent article by Erro et al. [1] ‘‘The eye of the tiger sign in pure akinesia with gait freezing’’ with great interest. The eye of the tiger sign is a neuroradiologic sign that reflects accumulated iron. This sign has been associated with neurodegeneration with brain iron accumulation type 1 (NBIA1), and mutations in the gene encoding pantothenate kinase 2 (PANK2) are known to be involved [2]. We recently experienced a patient with atypical parkinsonism who showed the eye of the tiger sign upon T2-weighted magnetic resonance imaging (MRI) of the brain. However, T2*-weighted MRI showed no abnormal lesions, and the eye of the tiger sign in our case turned out to be false. To our knowledge, our case is the first case of pseudo eye of the tiger sign and we need to consider the significance of T2*-weighted MRI findings in judging the validity of the eye of the tiger sign. A 76-year-old woman was admitted to our hospital because of progressive gait disturbances for more than 2 years. On neurological examination, she walked with short shuffling steps with stooped posture and presented difficulty while turning. She also showed postural instability and bradykinesia. In addition to her parkinsonian symptoms, she presented with urinary incontinence, severe constipation and gastric dysmotility. She did not show resting tremor, rigidity, dysphagia, dysarthria, ataxia, sensory disturbance, gaze palsy or orthostatic hypotension. In addition, her muscle strength and deep tendon reflex were normal. The results of a Mini-Mental State Examination (MMSE) revealed intact cognitive function. Although she was treated with L-dopa (up to 600 mg/day), her neurological symptoms persisted. T2-weighted MRI of the brain revealed high signal intensity in the globus pallidus surrounded by a ring of low signal intensity, the so-called eye of the tiger sign (Fig. 1a, b). However, she had no family history of neurological disorders and the results of hematological examinations, including iron, ferritin and ceruloplasmin, were all normal. Moreover, T2*-weighted MRI showed no accumulated iron in the affected regions (Fig. 1c). Therefore, we diagnosed the patient with atypical parkinsonism with pure akinesia, but not NBIA1. The eye of the tiger sign has been infrequently reported in neurodegenerative diseases other than NBIA1, including multiple system atrophy (MSA), pure akinesia and corticobasal degeneration (CBD) [1, 3, 4]. These reports suggest that the eye of the tiger sign is not always specific for NBIA1. On the other hand, the authors of these reports did not evaluate the deposition of iron as we did in our case. Therefore, whether neurodegenerative diseases other than NBIA1 manifest the eye of the tiger sign is not obvious, and the signs in previous reports may have been pseudo signs, as in our case. Although the cause of the pseudo eye of the tiger sign is unknown, it may reflect degeneration of the globus pallidus. Regardless, it is important to consider the existence of the pseudo eye of the tiger sign and confirm the deposition of iron.