Experimental expression of CCNF mutations identified from ALS/FTD patients led to defective protein degradation and signature features of ALS pathogenesis in vitro including elevated ubiquitylation and increased levels of ubiquitylated ribonucleotide reductase M2 (RRM2) and TDP-43 [15]. The gene discussed is RRM2; the disease is amyotrophic lateral sclerosis.