Given the high frequency of oncogenic activating mutations affecting the PI3K/AKT pathway in human tumours60, our data provide preclinical rationale suggesting that the inactivation of TROLL-2 and TROLL-3, the nuclear sequestration of WDR26, or interfering with the interaction between the TROLLs, WDR26 and AKT might be effective in halting cancer progression and resistance to AKT targeted therapy. The gene discussed is WDR26; the disease is cancer.