Mechanistically, SRSF3 mediates the alternative splicing of AMOTL1 to generate the oncogenic transcript AMOTL1-L, which is preferably localized in the intracellular compartment and has a robust interaction with YAP1 to promote its nucleus entry in NPC, thereby exhibiting tumorigenic potentials in NPC. The gene discussed is SRSF3; the disease is nasopharyngeal carcinoma.