Further analysis found high PD-L1 expression in all three patient tumours, a mutation in the STAT6 gene, amplification of a “neoantigen” Erb-B2 receptor tyrosine kinase 2 (ERBB2) along with DNA damage response in patient 2 and an intermediate tumour mutation burden (TMB) with 8.15 mutations per megabase in patient 3. The gene discussed is ERBB2; the disease is neoplasm.