Our study situates persulfidation within this framework as an inhibitor of GSK3β, similarly to previous reports in the context of Alzheimer's Disease [49], suggesting that it is a tractable redox modification capable of interfacing with canonical fate-setting pathways while highlighting the unmet need to connect discrete oxPTMs to genome-wide transcriptional programs. Here, GSK3B is linked to early-onset autosomal dominant Alzheimer disease.