Although we could not make such an association in cases with private event signatures dominated by APOBEC (Fig. 6; Supplementary Figure S5) or Polη (Figs. 6, 7), these data suggest that germline variants in a different subset of DNA repair genes may influence the acquisition of private somatic mutations during lung cancer progression, distinct from those associated with mutation burden in the founding clone. The gene discussed is POLH; the disease is lung carcinoma.