The mutations consisted of small in-frame deletions or substitutions clustered around the ATP-binding site in exons 18–21 of EGFR. Some investigators subsequently found that EGFR mutations are one of the strong determinants of tumour response to EGFR tyrosine kinase inhibitors (Pao et al, 2004; Han et al, 2005; Shigematsu et al, 2005). Here, EGFR is linked to neoplasm.