Taken together, our findings unveil a crucial role for ∆Np63 in driving a common oncogenic transcriptional programme essential for the formation and progression of both LUAD and LUSC, and identify BCL9L as an important mediator of the oncogenic effects of ∆Np63 in both NSCLC subtypes. The gene discussed is BCL9L; the disease is non-small cell lung carcinoma.