Lim et al. provided evidence on functional interaction between parkin and LIMK1 in human dopaminergic neuroblastoma-derived BE(2)-M17 cell line, where parkin overexpression enhances LIMK1-ubiquitination and reduces the level of LIMK1-induced cofilin phosphorylation [137]. Here, LIMK1 is linked to dopaminergic neuroblastoma.