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Hematopoietic stem cell transplantation (HSCT) remains a cornerstone in the management of patients with hematological malignancies. Endothelial injury syndromes, such as HSCT-associated thrombotic microangiopathy (HSCT-TMA), veno-occlusive disease/sinusoidal obstruction syndrome (SOS/VOD), and capillary leak syndrome (CLS), constitute complications after HSCT. Moreover, endothelial damage is prevalent after immunotherapy with chimeric antigen receptor-T (CAR-T) and can be manifested with cytokine release syndrome (CRS) or immune effector cell-associated neurotoxicity syndrome (ICANS). Our literature review aims to investigate the genetic susceptibility in endothelial injury syndromes after HSCT and CAR-T cell therapy. Variations in complement pathway- and endothelial function-related genes have been associated with the development of HSCT-TMA. In these genes, <i>CFHR5</i>, <i>CFHR1</i>, <i>CFHR3</i>, <i>CFI</i>, <i>ADAMTS13</i>, <i>CFB</i>, <i>C3</i>, <i>C4</i>, <i>C5</i>, and <i>MASP1</i> are included. Thus, patients with these variations might have a predisposition to complement activation, which is also exaggerated by other factors (such as acute graft-versus-host disease, infections, and calcineurin inhibitors). Few studies have examined the genetic susceptibility to SOS/VOD syndrome, and the implicated genes include <i>CFH, methylenetetrahydrofolate reductase</i>, and <i>heparinase</i>. Finally, specific mutations have been associated with the onset of CRS (<i>PFKFB4</i>, <i>CX3CR1</i>) and ICANS (<i>PPM1D</i>, <i>DNMT3A</i>, <i>TE2</i>, <i>ASXL1</i>). More research is essential in this field to achieve better outcomes for our patients.