CWF19L1 and aceruloplasminemia: A study only revealed the role of CWF19L1/hDrn 1 in an intron turnover after hDbr1 splicing,23 and a report corroborates that loss‐of‐function mutations in CWF19Ll lead to early onset cerebellar ataxia and (progressive) cerebellar atrophy.24