Indeed, SNX1 depletion in a non-small-cell lung cancer cells resistant to the EGFR inhibitor gefitinib showed a similar effect on Met and Erk1/2 phosphorylation.33 In similar cells overexpressing constitutively active Met, SNX2 depletion promotes the endocytosis of the receptor and its degradation.34 These conclusions seem also valid for other RTKs as work by Nguyen et al. 58 showed an increase in EGFR phosphorylation following SNX1 depletion in CRC cells. The gene discussed is MAPK3; the disease is non-small cell lung carcinoma.