This drug exploits the vulnerability of CAFs, which lack Mcl-1 expression and possess mitochondria in a “death-prepared state,” thereby suppressing the progression and metastasis of CCA.This approach offers a novel therapeutic strategy for treating CAF-rich solid tumors (66, 67).Additionally, preclinical studies implicate CAFs-derived matrix metalloproteinases (MMPs), TGF-β, and IL-6 as key drivers of immunosuppression and tumor progression (68). The gene discussed is IL6; the disease is cholangiocarcinoma.