Findings from the current and last decade reinforce the unifying hypothesis that put FTD and ALS in the group of the so-called proteinopathies by TDP-43, stating that TDP-43 abnormal accumulation is a shared molecular basis.9,31 Some of the known TDP-43 biochemical abnormalities include hyper-phosphorylation, ubiquitination, and truncation of its N-terminal portion. The gene discussed is TARDBP; the disease is amyotrophic lateral sclerosis.