Our findings suggest that a network of insulin signaling dysfunction, and low-grade inflammation, potentially with alterations in IGF-1 as the precipitating event, similar to IGF-1's pleiotropic roles in other clinical conditions, partially contribute, directly or indirectly, to the objective cognitive impairments and other subjective QoL functions in young adults with CP (66, 67). This evidence concerns the gene INS and Cognitive impairment.