Our results indicate that the absence of CK18 in CTCs was not a consequence of the CK18-iFISH methodology itself, which is in agreement with the concept that tumor cells may regulate CK18 expression under certain circumstances, and such post-translational modulation of CK18 protein in CTCs revealed and quantified by phenotypic immunostaining is of particular biological and clinical significance. This evidence concerns the gene KRT18 and neoplasm.