SLC9A8 and amyotrophic lateral sclerosis: First, in the molecular level one typical pathological hallmark for neurodegeneration of ALS (e.g., tau, amyloid, and beta-protein precursor) is the change in cell cycle control and progression, which can be regulated by SLC9A8 by inhibiting Na+/H+ exchanger activity in epithelia (Hu et al., 1998; Orlowski and Grinstein, 2004).