Retinitis Pigmentosa (RP) is a class of hereditary retinal dystrophy associated with gradual visual failure and a subsequent loss of light-sensitive cells in the retina, leading to blindness. Many mutated genes were found to be causative of this disease. Despite a number of compiling efforts, the process of cell death in photoreceptors remains to be clearly elucidated. We recently reported an abnormal cell cycle reentry in photoreceptors undergoing degeneration in Rd1 mice, a model of RP, and identified the polycomb repressive complex 1 (PRC1) core component BMI1 as a critical molecular factor orchestrating the cell death mechanism. As the cell death rescue in Rd1;Bmi-1 KO mice was independent on the conventional Ink4a/Arf pathways, we now explored the structural properties of BMI1 in order to examine the differential expression of its posttranslational modifications in Rd1 retina. Our results suggest that BMI1 cell death induction in Rd1 is not related to its phosphorylation status. We therefore propose the epigenetic activity of BMI1 as an alternative route for BMI1-mediated toxicity in Rd1.