Whilst the molecular link between Usp9x and Kras remains to be revealed, reduced expression of the USP9X substrate ITCH was observed in PDA cells lacking USP9X, and ITCH overexpression could rescue the transformation and anoikis phenotype, together suggesting ITCH as a likely mediator of USP9X tumour suppressor function [95]. The gene discussed is KRAS; the disease is Patent ductus arteriosus.