A number of small-molecule inhibitors acting on E3 Ub ligase complexes have already been identified as promising drug targets in cancer (63), and considering that free Ub levels were improved by altering the E3 ligase activity of the CCNF complex, modulating this activity may represent a potential therapeutic avenue for the treatment of CCNF-associated ALS. The gene discussed is CCNF; the disease is amyotrophic lateral sclerosis.