Clonal hematopoiesis is causally associated with an increased risk of cancer and all-cause mortality, and loss of function in hematopoietic cells and mutations in macrophages accelerate CVD [43]; Interleukin-1β mediates inflammation in the tumor microenvironment and stimulates downstream interleukin-6 receptor signaling pathway to develop CVD [44, 47]; Vascular endothelial growth factor is associated with abnormal endothelial function, angiogenesis, and hemodynamic effects and is often highly expressed in cancer and CVD [45]. The gene discussed is VEGFA; the disease is neoplasm.