In contrast, the PDK1 L155E mice were embryonically lethal, and Cre-mediated bypass of the lethal period by targeting the expression of the mutant PDK1 L55E protein to the brain led to neurodevelopmental disorders and disrupted behavior, thereby highlighting the importance of the Akt-independent actions of this signaling toolkit regarding brain development and function (Bayascas et al., 2008). This evidence concerns the gene AKT1 and neurodevelopmental disorder.