This modification impairs TDP‐43's ability to bind RNA and leads to the accumulation of insoluble, hyper‐phosphorylated forms of the protein, which resemble the pathological inclusions found in conditions like amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP‐43 inclusions (FTLD‐TDP) (Cohen et al. 2015). The gene discussed is TARDBP; the disease is frontotemporal dementia.