Our observation that USP4 is recruited by TRPS1 to de-ubiquitinate HDAC2 and silence USP4, resulting in inhibition of tumor cell growth by TRPS1, is consistent with these notions elucidating the underlying molecular details of the oncogenic function of the TRPS1/HDAC2/USP4 axis in tumor growth. The gene discussed is TRPS1; the disease is neoplasm.