In addition, some newer animal models of infantile spasms have been reported recently, including dysfunction (knockout) of the adenomatous polyposis coli (APC) pathway leading to elevated beta-catenin, causing abnormal brain development [16]; pathogenic microbiome alterations [17]; and mechanistic target of rapamycin (mTOR) pathway abnormalities [18]. The gene discussed is APC; the disease is infantile spasms.