Overexpression of METTL1-WDR4 causes malignizationof mouse embryonic fibroblasts while METTL1 knock-down or knock-outsuppresses tumor growth in several xenograft tumor models.19 The increased expression of METTL1 was recentlycorrelated with unfavorable prognosis in lung and hepatocellular carcinomasacting via the AKT/mTORC1 and PTEN pathways, respectively.20,21 Importantly, several publications have linked METTL1-WDR4 dysregulationto carcinogenesis22 suggesting that targetingthe complex hold great promise for the development of chemical probesand chemotherapeutic drugs. The gene discussed is AKT1; the disease is neoplasm.