We observed that fragments harboring tumor-specific TP53 mutations in the circulation were significantly shorter than fragments harboring TP53 variants associated with clonal hematopoiesis (p < 0.001, Kolmogorov–Smirnov test), as well as fragments harboring wild-type TP53 coding regions (p < 0.001, Kolmogorov–Smirnov test) (Fig. 2h; Supplementary Data 7–9). The gene discussed is TP53; the disease is neoplasm.