Previous studies also reported no increase in spontaneous tumor formation in SAMHD1‐deficient mice, possibly due to low DNA damage levels controlled by p53‐mediated responses, indicating that SAMHD1 knockout is not linked to a strong mutator phenotype.[47] We propose that the growth inhibition seen with SAMHD1 overexpression results from gradual cell cycle slowing, rather than an acute effect typical of strong cell cycle inhibitors. The gene discussed is TP53; the disease is neoplasm.