These findings suggest the following conclusions: (1) overexpression of ABCG2 by cancer cells may promote resistance to EGFR TKIs, (2) the Q141K variant of ABCG2 could cause differences in the pharmacokinetics of EGFR TKIs (except afatinib), and (3) EGFR TKIs may induce drug interactions by inhibiting both wild-type and variant ABCG2. The gene discussed is EGFR; the disease is cancer.