Halepoto et al. (2015) demonstrated that children with autism have higher serum levels of Shh than normal children, that is, there is a link between abnormal shh signaling pathway and autism. Under stress conditions, SHH ligands do not bind to the receptor for Patch1, Patch1 still inhibits the SMO and GLI1 is unable to be activated by SMO, resulting in down-regulation of SMO-SHH signaling and abnormal increase in oxidative stress and neuronal inflammation leading to the development of autism (Rahi and Mehan, 2020). The gene discussed is SMO; the disease is autism.