While the prevalence of age-related clonal hematopoiesis in individuals >50 years of age has been widely studied, the knowledge of clonal hematopoiesis in younger individuals is critically lacking. It is well known that the genes commonly mutated in adult AML (e.g. DNMT3A, TET2) are very rarely mutated in pediatric AML, suggesting that not only is the prevalence of clonal mutation different as a function of age, but also the genetic targets of clonal mutation. Such knowledge is critical as efforts to develop and implement precision therapeutics for a host of hematological diseases continue to expand. The background mutational profile is essential. This study would be the first to systematically examine the mutational spectrum using a high-resolution sequencing method with a limit of detection of 0.0001 in age-appropriate genes recurrently associated with AML in healthy children and young adults. Several studies in the past that utilized low-throughput methods found somatic mutations in genes such as JAK2 and TP53 in individuals without hematologic disease. Individuals with these mutations are associated with an increased risk of developing hematological and cardiovascular diseases in later in life. Once the background clonal hematopoiesis in healthy individuals is established and characterized, such profile can be used as a comparison point to hematological disease of genetic nature. For example, in some clinical cases involving hematopoietic stem cell transplantation (HCT), low frequency somatic mutations are present in healthy donors, which seemed to be under neutral selection in the donor’s body, but were subsequently implicated in the onset of secondary leukemia (with a reported incidence of 0.001) in the recipient as a result of clonal expansion, suggesting positive selection for putative pre-leukemic clones. Establishing the prevalence and the mutational spectrum of clonal hematopoiesis of blood and marrow donors would be crucial to understanding the clonal dynamics and selection of many rare donor clones in recipients post-HCT. In the subsequent follow-up study, we would identify somatic mutations that could be linked to the development of secondary hematologic complications (e.g. myelodysplasia, donor-derived leukemia, graft vs host disease) in recipients post-HCT, and with such data, we aim to better inform transplantation therapy in order to minimize the risk of secondary hematologic complications in the recipients.