Whole-genome linkage analysis and genome sequencing identified CCNF to be linked to both familial and sporadic ALS patients. "In vitro" and "in vivo" studies using ALS-linked mutations in CCNF were also carried out. It was found that certain CCNF mutations caused increased ubiquitylation activity of cyclin F  leading to abnormal ubiquitylation of proteins. In zebrafish, mutant CCNF fish showed motor neuron axonopathy and reduced motor response. Cyclin F has a tumor suppressor role because normal expression is involved in cell cycle regulation by inducing G2 arrest and preventing mitosis. Moreover, cyclin F through RRM2 and CP110 control centrosome duplication and reduce the frequency of genomic mutations. So far, mutations in CCNF and increased RRM2 expression have been identified in several human cancers.