The SEACAT and the Iml1 complex are functionally conserved in humans. To date, somatic mutations in the human IML1/SEA1 homolog, DEPDC5, have been found mutated in cancers (Bar-Peled et al. 2013) and germline mutations have been found in familial autosomal-dominant epilepsy and focal malformations of cortical development (Dibbens et al. 2013; Ishida et al. 2013; Martin et al. 2013; Picard et al. 2014; D’Gama et al. 2015). It is anticipated that homologs of other members of the SEA complex, including SEA3, will also prove to be clinically relevant.