A panel of genes that, when mutated, had previously been correlated with response to cisplatin-based chemotherapy or PD-1/PD-L1 blockade (ERCC2, RB1, ATM and FANCC)15–22, as well as increased TMB (using an established cutpoint of ≥10 mutations per megabase (mut/Mb), which has served as the basis for tumor-agnostic PD-1 blockade regulatory approvals and for which sensitivity and specificity in bladder cancer has been established23,24), was pre-specified for analysis. The gene discussed is ATM; the disease is neoplasm.