In contrast to NTHL1-deficient tumors, in none of the tumors of the carriers was mutational signature SBS30 the main signature, because it was only present in 1 tumor, where it had a minor contribution (Figure 1B and Supplementary Table 2).4 These observations indicate that biallelic inactivation of NTHL1 through a somatic second hit was not evident and that monoallelic inactivation of NTHL1 was insufficient to result in the accumulation of somatic mutations that are characteristic of an NTHL1-deficiency phenotype. Here, NTHL1 is linked to neoplasm.