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The neuropathological correlate of FTD is frontotemporal lobar degeneration (FTLD), characterized by tau-, TDP-43-, and FUS-immunoreactive neuronal inclusions. An earlier discovery that a hexanucleotide repeat expansion mutation in chromosome 9 open reading frame 72 (<jats:italic>C9orf72<\/jats:italic>) gene causes ALS and FTD established a special subtype of ALS and FTLD with TDP-43 pathology (C9FTD\/ALS). Normal individuals carry 2\u201310 hexanucleotide GGGGCC repeats in the <jats:italic>C9orf72<\/jats:italic> gene, while more than a few hundred repeats represent a risk for ALS and FTD. The proposed molecular mechanisms by which <jats:italic>C9orf72<\/jats:italic> repeat expansions induce neurodegenerative changes are C9orf72 loss-of-function through haploinsufficiency, RNA toxic gain-of-function, and gain-of-function through the accumulation of toxic dipeptide repeat proteins. However, many more cellular processes are affected by pathological processes in C9FTD\/ALS, including nucleocytoplasmic transport, RNA processing, normal function of nucleolus, formation of membraneless organelles, translation, ubiquitin proteasome system, Notch signalling pathway, granule transport, and normal function of TAR DNA-binding protein 43 (TDP-43). Although the exact molecular mechanisms through which <jats:italic>C9orf72<\/jats:italic> repeat expansions account for neurodegeneration have not been elucidated, some potential therapeutics, such as antisense oligonucleotides targeting hexanucleotide GGGGCC repeats in mRNA, were successful in preclinical trials and are awaiting phase 1 clinical trials. 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