By using DNA- and RNA-directed lung-cancer sequencing panels to compare the three FGFR1 inhibition-resistant single clones with their sensitive parental control cell line (NCI-H1581) we could exclude several known mechanisms of AKT activation, e.g., AKT, RAS, PTEN, PIK3CA or FGFR1 gatekeeper mutations, overexpression of AKT, FGFR1 or activation of MET (Fig. 3e and S3d, e). The gene discussed is MET; the disease is lung carcinoma.