Chimeric antigen receptor (CAR) T cell therapies have significantly improved treatment outcomes for various hematologic malignancies, but they also carry significant risks, including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and other toxicities. This review discusses the underlying pathophysiological mechanisms and provides guidelines for grading and managing these toxicities. **CRS** is characterized by fever, hypotension, and end-organ dysfunction, often occurring within 14 days of infusion. Inflammatory markers and cytokines such as TNF-α, IL-1, and IL-6 are implicated. Endothelial activation and inflammation play a crucial role in CRS severity. Factors like higher CAR T cell dose, CD28 costimulation, and pre-existing disease burden increase the risk of severe CRS. Management involves supportive care, tocilizumab, and corticosteroids, with more intensive interventions for severe cases. **ICANS** is a central nervous system disorder with symptoms like aphasia, altered consciousness, and seizures. It can occur concurrently with CRS or independently. Elevated cytokines and endothelial activation are key factors. Higher pre-infusion m-EASIX scores and thrombocytopenia are risk factors. Grading is based on the Immune Effector Cell-Associated Encephalopathy (ICE) score, with supportive care and corticosteroids being the mainstays. Anakinra, ruxolitinib, and dasatinib are potential treatments for refractory cases. Other neurotoxicities distinct from ICANS, such as movement disorders and cognitive impairments, have also been observed. Early intervention and prophylactic strategies are being explored to mitigate these toxicities.Chimeric antigen receptor (CAR) T cell therapies have significantly improved treatment outcomes for various hematologic malignancies, but they also carry significant risks, including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and other toxicities. This review discusses the underlying pathophysiological mechanisms and provides guidelines for grading and managing these toxicities. **CRS** is characterized by fever, hypotension, and end-organ dysfunction, often occurring within 14 days of infusion. Inflammatory markers and cytokines such as TNF-α, IL-1, and IL-6 are implicated. Endothelial activation and inflammation play a crucial role in CRS severity. Factors like higher CAR T cell dose, CD28 costimulation, and pre-existing disease burden increase the risk of severe CRS. Management involves supportive care, tocilizumab, and corticosteroids, with more intensive interventions for severe cases. **ICANS** is a central nervous system disorder with symptoms like aphasia, altered consciousness, and seizures. It can occur concurrently with CRS or independently. Elevated cytokines and endothelial activation are key factors. Higher pre-infusion m-EASIX scores and thrombocytopenia are risk factors. Grading is based on the Immune Effector Cell-Associated Encephalopathy (ICE) score, with supportive care and corticosteroids being the mainstays. Anakinra, ruxolitinib, and dasatinib are potential treatments for refractory cases. Other neurotoxicities distinct from ICANS, such as movement disorders and cognitive impairments, have also been observed. Early intervention and prophylactic strategies are being explored to mitigate these toxicities.