In order to determine if the impaired trafficking of EGFR was a direct consequence of the kinase mutation or a result of “saturation” of the endosomal-lysosomal pathway 18 from a hyperactive kinase and excessive EGFR, we compared the transit of EGFR in A431 (a carcinoid cell line carrying EGFR WT and displaying high expression of EGFR as well as exquisite sensitivity to EGFR tyrosine kinase inhibitor (TKI)) to that in PC9 cells 19. This evidence concerns the gene EGFR and carcinoid tumor.