Also, models of hematopoietic Tet2 deletion suggests that Tet2‐mutant myeloid cells produce higher levels of S100a8/S100a9, which enhance vascular endothelial growth factor A (VEGF‐A) production by cancer cells, leading to increased tumor vasculature and growth in subcutaneously transplanted lung cancer [48]. The gene discussed is TET2; the disease is neoplasm.