To assess the impact of DUSP22 expression in suppressing the EGFR/ERK signaling pathway on the growth of EGFR-TKI-resistant H1650 cells with sustained Akt activation, we observed a significant inhibitory effect of DUSP22 on H1650 xenograft tumor growth in SCID (severe combined immunodeficiency disease) mice (Fig. 3H, I), suggesting that DUSP22-mediated inhibition of the EGFR pathway at multiple levels could be highly effective against TKI-resistant PTEN-deleted H1650 cells. The gene discussed is AKT1; the disease is severe combined immunodeficiency.