Although we cannot rule out the possible existence of minor subclones below the detection limit of our sequencing assays, and subsequent clonal outgrowth of such minor TP53 mutant HSPC clones during SAR405838 treatment, if TP53 mutant alleles in cfDNA had indeed originated primarily from TP53 mutant HSPCs, it is unlikely we would have observed the correlation between TP53 mutation burden and tumour growth (Fig. 2e). This evidence concerns the gene TP53 and neoplasm.