FLT4是致癌基因，编码蛋白是细胞表面受体，其是血管内皮生长因子（VEGF）途径的成员，其参与肿瘤血管生成。VEGF配体，VEGF-C或VEGF-D与FLT4的结合激活信号传导途径，其反过来介导白血病中的细胞增殖，存活，侵袭和对化学疗法的抗性。此外，FLT4是淋巴管生成的关键调节因子，是维持淋巴管内皮所必需的。FLT4的胚系突变与遗传性Nonne-Milroy病相关，其是IA型原发性淋巴水肿的常染色体显性形式。已在多种肿瘤类型中观察到异常FLT4表达，包括肺腺癌和结直肠癌等，并且在透明细胞肾细胞癌中高度甲基化。然而，FLT4的体细胞突变在人类癌症中并不常见，在结直肠癌，前列腺癌和肺癌等肿瘤类型中发现了FLT4的点突变，移码缺失或过表达。

FLT4 (also VEGFR3) is a cell surface receptor that is a member of the vascular endothelial growth factor (VEGF) pathway. Binding of the VEGF ligands, VEGF-C or VEGF-D, to FLT4 activates pathway signaling, which in turn mediates cell proliferation, survival, invasion, and resistance to chemotherapy in leukemia. In addition, FLT4 is a critical regulator of lymphangiogenesis and is necessary for the maintenance of the lymphatic endothelium. Germline mutations in FLT4 have been identified in hereditary Nonne-Milroy disease, an autosomal dominant form of primary lymphedema type IA. Aberrant FLT4 expression has been observed in several tumor types including lung adenocarcinoma and colorectal adenocarcinoma, among others, and has been shown to be hypermethylated in clear cell renal cell carcinomas.

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