Lieshout et al. (2023) showed that IL-17A promotes tumor cell proliferation in PSC-associated CCA organoids, suggesting the IL-17A axis as a potential immune therapeutic target for this disease subtype. Similarly, Li Z. et al. (2024) found that hepatitis B virus infection suppresses antitumor immunity through the TNFSF9 pathway, and inhibition of TNFSF9 enhances treatment sensitivity, unveiling a novel mechanism of immune modulation in virus-associated iCCA. The gene discussed is IL17A; the disease is hepatitis B virus infection.