KRAS and adenocarcinoma: Despite contributing a significant number of mutations in adenocarcinomas (Fig. 2d), APOBEC-associated signatures SBS2 and SBS13 generate a significantly lower number of driver mutations in EGFR, TP53, and KRAS (OR=0.28; p-value=2.8 × 10−14) in comparison to their prevalence in the overall adenocarcinoma cohort, with most APOBEC-associated mutations being TP53 point mutations in a small number of samples (Fig. 2g).