Recent work by Tebbenkamp et al. [19] provides evidence that DNAJC30 contributes to Williams syndrome pathogenesis via a mitochondrial-based mechanism, but also implicates LIMK1 as a potential contributor, since DNAJC30 and LIMK1 are identified as part of a shared functional cluster of genes, based on co-expression and protein-to-protein interaction networks. The gene discussed is LIMK1; the disease is Williams syndrome.