Based on limited published evidence, KICS2 is a subunit of the KICSTOR complex that regulates mTORC1 signaling in response to amino acid and glucose availability. KICS2 localizes to lysosomes where it recruits the GATOR1 complex, enabling its interaction with RAG GTPases and GATOR2, thereby negatively regulating mTORC1 when nutrients are depleted 1. Bi-allelic KICS2 mutations impair KICSTOR complex formation and nutrient-dependent mTORC1 regulation, affecting translation, splicing, and ciliogenesis pathways 2. Loss of KICS2 function leads to constitutive mTORC1 activation and causes autosomal recessive intellectual disability with epilepsy 2.