The SYK tyrosine kinase plays a crucial role in diverse biological functions beyond its traditional role in adaptive immune signaling. It is involved in cellular adhesion, innate immune recognition, osteoclast maturation, platelet activation, and vascular development. SYK is activated by C-type lectins and integrins, and activates pathways such as the CARD9/CARMA1–BCL10–MALT1 and NLRP3 inflammasome. Drosophila studies suggest an ancient evolutionary origin of SYK signaling. SYK is crucial in autoimmune diseases and hematological malignancies. This review summarizes current understanding of SYK functions and their therapeutic implications. SYK is a 72 kDa non-receptor tyrosine kinase with two SH2 domains and a kinase domain. It is highly expressed in hematopoietic cells and is involved in B and T cell development. SYK deficiency leads to the absence of mature B cells, while ZAP70 deficiency causes severe T cell defects. SYK is also required for FcεRI signaling in mast cells and FcγR signaling in neutrophils and macrophages. ZAP70 is expressed throughout B cell development and participates in pre-BCR signaling. SYK is also involved in mast cell and neutrophil functions. SYK signaling is mediated through ITAMs, which are phosphorylated upon receptor engagement. ITAM-based signaling is involved in BCR, TCR, and FcR signaling. SYK activates downstream pathways including Ca²+ and PKC signaling, RAS homologue (RHO)-family, Pyk2-mediated cytoskeletal rearrangement, reactive oxygen species (ROS) production, and phagocytosis. SYK also participates in innate immune functions such as fungal recognition and pathogen recognition through C-type lectins. SYK is involved in integrin and selectin signaling, which are crucial for leukocyte adhesion and migration. SYK is also involved in the recognition of dead cells and in the activation of the NLRP3 inflammasome. SYK plays a role in bacterial and viral recognition, as well as in the pathogenesis of diseases such as allergy, autoimmunity, and hematological malignancies. SYK inhibitors have shown promise in treating these diseases. SYK is also involved in non-immune functions such as bone metabolism, platelet functions, and vascular development. It is required for osteoclast development and function, and for the separation of lymphatic vessels from the general circulation. SYK is expressed in non-hematopoietic tissues and may have an ancient evolutionary origin. SYK is involved in the development of various tumors, including hematological malignancies and non-hematopoietic tumors. SYK is a promising therapeutic target for the treatment of various diseases, including autoimmune disorders and hematological malignancies. However, the long-term use of SYK inhibitors mayThe SYK tyrosine kinase plays a crucial role in diverse biological functions beyond its traditional role in adaptive immune signaling. It is involved in cellular adhesion, innate immune recognition, osteoclast maturation, platelet activation, and vascular development. SYK is activated by C-type lectins and integrins, and activates pathways such as the CARD9/CARMA1–BCL10–MALT1 and NLRP3 inflammasome. Drosophila studies suggest an ancient evolutionary origin of SYK signaling. SYK is crucial in autoimmune diseases and hematological malignancies. This review summarizes current understanding of SYK functions and their therapeutic implications. SYK is a 72 kDa non-receptor tyrosine kinase with two SH2 domains and a kinase domain. It is highly expressed in hematopoietic cells and is involved in B and T cell development. SYK deficiency leads to the absence of mature B cells, while ZAP70 deficiency causes severe T cell defects. SYK is also required for FcεRI signaling in mast cells and FcγR signaling in neutrophils and macrophages. ZAP70 is expressed throughout B cell development and participates in pre-BCR signaling. SYK is also involved in mast cell and neutrophil functions. SYK signaling is mediated through ITAMs, which are phosphorylated upon receptor engagement. ITAM-based signaling is involved in BCR, TCR, and FcR signaling. SYK activates downstream pathways including Ca²+ and PKC signaling, RAS homologue (RHO)-family, Pyk2-mediated cytoskeletal rearrangement, reactive oxygen species (ROS) production, and phagocytosis. SYK also participates in innate immune functions such as fungal recognition and pathogen recognition through C-type lectins. SYK is involved in integrin and selectin signaling, which are crucial for leukocyte adhesion and migration. SYK is also involved in the recognition of dead cells and in the activation of the NLRP3 inflammasome. SYK plays a role in bacterial and viral recognition, as well as in the pathogenesis of diseases such as allergy, autoimmunity, and hematological malignancies. SYK inhibitors have shown promise in treating these diseases. SYK is also involved in non-immune functions such as bone metabolism, platelet functions, and vascular development. It is required for osteoclast development and function, and for the separation of lymphatic vessels from the general circulation. SYK is expressed in non-hematopoietic tissues and may have an ancient evolutionary origin. SYK is involved in the development of various tumors, including hematological malignancies and non-hematopoietic tumors. SYK is a promising therapeutic target for the treatment of various diseases, including autoimmune disorders and hematological malignancies. However, the long-term use of SYK inhibitors may