STRADA (STE20-related adaptor alpha) is a pseudokinase that functions as a critical regulator of the mechanistic target of rapamycin (mTOR) pathway. STRADA operates as a catalytically inactive protein that forms a complex with CAB39/MO25 to bind and activate the tumor suppressor LKB1, promoting its conformational change to an active state 1. This LKB1-STRADA interaction enables LKB1 to phosphorylate and activate downstream AMP-activated protein kinase family members, which regulate cellular energy sensing and proliferation 1. Biallelic pathogenic STRADA mutations cause Pretzel Syndrome (PMSE), an autosomal recessive mTORopathy characterized by polyhydramnios, megalencephaly, drug-resistant epilepsy, and severe developmental delay 23. Loss of STRADA function results in mTOR pathway hyperactivation during cortical development, leading to delayed neurogenesis, excessive neural stem cell and outer radial glia expansion, and abnormal primary cilia architecture 24. In ventral forebrain development, STRADA deficiency causes delayed interneuron differentiation with altered cell fate specification 4. Clinically, mTOR pathway inhibitors like sirolimus and rapamycin show therapeutic potential in STRADA deficiency, offering promise for ameliorating seizures and neurodevelopmental abnormalities 34. Additionally, STRADA expression is downregulated during sevoflurane postconditioning-mediated cardioprotection against hypoxia-reoxygenation injury 5.