Considering the evidence that ibrutinib is highly potent in in vitro for EGFR mutant NSCLC cancer cell lines but only moderately slow down tumor progression in the mouse model, we propose that without alteration of the PK property of Ibrutinib itself, a specially designed formulation or dosage which can help sustain effective concentration should be considered to achieve the efficacy in the clinic application for mutant EGFR driven NSCLC. The gene discussed is EGFR; the disease is neoplasm.