Indeed, we found a strong replicational bias (average 1.38-fold of all six mutational classes in XP-C leukemia, Wilcoxon signed-rank test, two-sided, P = 2.91e−11) compatible with preferential bypass of purine DNA lesions by error-prone TLS polymerases on the lagging strand (Fig. 4b and Supplementary Fig. 4c) in XPC-deficient tumors. Here, XPC is linked to Xeroderma pigmentosum complementation group C.