Studies of aberrant insulin-like peptide (ILP) signaling in FXS originated from elevated phosphatase and tensin (PTEN), target of rapamycin (TOR), phosphoinositide 3-kinase (PI3K), and activated protein kinase B (Akt) in FXS model and patient neurons (Sharma et al., 2010; Hoeffer et al., 2012; Gross et al., 2015), consistent with elevated insulin signaling discovered in from transcriptome profiling of the mouse FXS model hippocampus (Prilutsky et al., 2015). Here, AKT1 is linked to fragile X syndrome.