Consistently, ectopic expression of the myristoylated form of AKT1 (myr-AKT1) significantly repressed USP12 expression in both human and mouse tumour cells (Fig. 1k); knockdown of endogenous AKT1 or AKT2, the two major isoforms of AKT, induced higher levels of USP12 than did the control treatment (Fig. 1l). The gene discussed is AKT1; the disease is neoplasm.