C9orf72 and amyotrophic lateral sclerosis: But interestingly, Nookala et al. (2012) did reveal that the crystal structure for the C-terminal fragment of FLCN, contained a DENN (differentially expressed in normal and neoplastic cells) domain that was highly similar to the DENN domain of the C9orf72 protein (Nookala et al., 2012), whose dominant expansion of a noncoding GGGGCC hexanucleotide repeat has been proven to be causative of both ALS and FTD (DeJesus-Hernandez et al., 2011).