Alternatively, the aberrant ubiquitination induced by increased CCNF activity (due to transgenic overexpression) may have resulted in progressive insolubility of TDP‐43, and eventually in the formation of inclusions, similar to ubiquitinated TDP‐43 inclusions found in ALS, as TDP‐43 is a ubiquitylation substrate of the CCNF complex [40]. Here, CCNF is linked to amyotrophic lateral sclerosis.