Toxoplasma gondii, a protozoan parasite, causes toxoplasmosis, a widespread zoonotic and food-borne disease that poses significant risks, particularly in opportunistic and congenital cases. This obligate intracellular parasite is highly prevalent worldwide, largely due to its versatile life cycle, involving multiple hosts and transmission routes, and its ability to establish chronic infections. The presence of this neurotropic parasite in the brain poses a reactivation risk in immunocompromised individuals and is associated with a higher likelihood of developing mental disorders. However, the role of the dormant bradyzoite stage in the pathophysiology of the disease is underexplored, mainly due to the lack of non-invasive detection methods and serologic tests targeting bradyzoite- or cyst-specific antigens. In tachyzoites, MORC partners with histone deacetylase HDAC3 to restrict chromatin access to transcription machinery at genes specific to the sexual and chronic stages. Depletion of MORC results in significant transcriptional changes, leading to the expression of a large repertoire of bradyzoite-specific genes, encompassing up to 50% of the chronic sub-transcriptome. We hypothesized that reducing MORC levels could be an effective strategy to discover new immunogenic bradyzoite markers. To test this, we identified bradyzoite proteins inducing immunoreactivity of sera from chronically infected, BCLA-positive mice.