Post-translational modifications (PTMs) represent an attractive mechanism, as many proteins implicated in AD (e.g., β-amyloid and tau) and non-AD neuropathologies (e.g., α-synuclein and TDP43) undergo PTMs (Marcelli et al., 2018; Pajarillo et al., 2019; Schaffert and Carter, 2020). This evidence concerns the gene TARDBP and Alzheimer disease.