Jusakul et al. analyzed 489 CCA cases from different regions [29] and found that liver fluke-associated CCAs frequently exhibited ERBB2 amplification and TP53 mutations, whereas non-fluke-associated cases demonstrated a higher prevalence of copy number alterations, elevated PD-1/PD-L2 expression, IDH1/2 and BAP1 mutations, and FGFR rearrangements with epigenetic dysregulation. The gene discussed is ERBB2; the disease is cholangiocarcinoma.