SBK2 (SH3 domain binding kinase family member 2) is a serine/threonine protein kinase with dual roles in inflammation and cardiac development. In the immune system, SBK2 functions as a critical negative regulator of atherosclerosis by phosphorylating NLRP3 inflammasome at Ser161, triggering Tollip-dependent autophagic degradation and subsequent inflammasome inactivation 1. This phosphorylation event represents the sole known kinase-driven mechanism for selective NLRP3 clearance, suppressing pro-inflammatory IL-1β/IL-18 secretion. In cardiac tissue, SBK2 is atrium-enriched and localized to sarcomere A-bands, where it maintains sarcomeric organization and integrity during cardiomyocyte differentiation 2. SBK2 knockdown causes loss of sarcomeric structure and decreased sarcomeric gene expression in neonatal and adult cardiomyocytes. Therapeutically, SBK2 is being investigated as a tumor imaging target; the SBK2 peptide specifically recognizes PTPmu-derived biomarkers on glioblastoma cells, enabling fluorescence and MRI-guided surgical resection 34. Additionally, SBK2 methylation patterns in cord blood show associations with immune pathway regulation following prenatal pet exposure 5. These findings identify SBK2 as a potential therapeutic target for atherosclerosis management and cardiac disease.