For the 12 patients who were stratified as HRDpos and experienced stable disease as best radiologic response, three tumor samples had a competitive gain-of-function alteration in an oncogene (missense mutation in EGFR, amplification of MYC and AKT2), and two samples had a pathogenic variant in a tumor suppressor gene (a frameshift mutation in KDM5C and a predicted splice variant of TSC1, respectively). The gene discussed is EGFR; the disease is neoplasm.