Childhood ALL exhibits a peak in incidence at the age of 2–5 years, and several experiments have demonstrated that chromosomal abnormalities detected at diagnostic were also identified at birth (such as ETV6-RUNX1, RUNX1-RUNX1T1, and PML-RARA gene fusions, as well as high hyperdiploidy), providing strong support to the prenatal origin of many childhood leukemia subtypes [4,5,6,7,8]. Here, RUNX1 is linked to childhood leukemia.