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). This evidence concerns the gene PTEN and fragile X syndrome.