ULK4 (unc-51 like kinase 4) is a serine/threonine kinase that functions primarily as a pseudokinase 1, acting as a scaffold protein rather than an active phosphotransferase 2. ULK4 regulates neuritogenesis and neuronal motility by modulating microtubule cytoskeleton organization and controlling multiple signaling pathways including ERK, p38, PKC, and JNK 3. At the ciliary tip, ULK4 undergoes phosphorylation-dependent SUMOylation that drives its self-assembly into biomolecular condensates, which recruit substrate proteins like Gli2 to transduce Hedgehog signaling during development 4. ULK4 has significant disease relevance across multiple conditions. Recurrent deletions of ULK4 are enriched in schizophrenia and bipolar disorder patients 3, with targeted Ulk4 deletion causing corpus callosum agenesis in mice. ULK4 is also implicated in lacunar stroke pathogenesis through GWAS and transcriptome-wide association studies, with expression variation associated with disease risk 5. Additionally, ULK4 genetic variants influence monoclonal gammopathy of undetermined significance risk through autophagy modulation and B-cell differentiation 6. The recently discovered CHR3 gene, unique to humans, incorporates ULK4-derived sequences and modulates cholinergic anti-inflammatory pathways 7. These findings suggest ULK4 represents a promising therapeutic target for neuropsychiatric and vascular disorders.