Ataxia is a prominent symptom of the X-linked neurodevelopmental/neurodegenerative disorder Christianson Syndrome (CS). A hallmark of ataxia disorders is the death of Purkinje Cells where Purkinje Cell cerebellar location can influence their vulnerability. Purkinje Cells express certain molecules in a highly patterned manner across the cerebellum, the most studied being aldolase C/zebrin-II (zebrin), expressed in parasagittal stripes across the cerebellum. We investigated if either type of Purkinje Cell was more vulnerable in CS using immunohistochemistry, looking specifically at motor lobules, anterior lobule III and posterior lobule VIII. We found that zebrin patterning appears normal before disease onset in CS mice followed by a narrow and aggressive window (10 days) of vulnerability in the anterior lobe of CS mice, arising at a similar time as the first firing alterations. The vulnerability affects only zebrin-negative Purkinje Cells, with zebrin-positive Purkinje Cells showing striking resilience. In contrast, all posterior Purkinje Cells were equally susceptible to degeneration at later disease stages. As Purkinje Cells are the only cerebellar cortex outputs and send their axons to the cerebellar nuclei (CN), we analyzed Purkinje Cell input onto the CN. Similarly, we found decreased zebrin-negative input onto large neurons in anterior CN. In contrast, zebrin-negative inputs onto posterior CN neurons and zebrin-positive inputs onto both anterior and posterior CN neurons were resilient. Our results suggest that both cerebellar location and zebrin molecular identity play a role in Purkinje Cell vulnerability in CS.