In the presence of high activation of the JAK-STAT pathway, the combination of a JAK inhibitor with an FGFR inhibitor enables tumor cells to switch from a drug-resistant phenotype (e.g., EMT) back to the luminal state with high AR expression, thereby restoring sensitivity to androgen receptor inhibitors (Chan et al., 2022; Deng et al., 2022). The gene discussed is SOAT1; the disease is neoplasm.