An alternative explanation for the cetuximab resistance in breast cancer cells was reported by Li et al. [104], who showed that breast tumor kinase (Btk)/protein-tyrosine kinase 6 (PTK6), a non-receptor, as well as a non-Src family PTK, which was originally identified in human melanocytes, is highly expressed in most human breast cancers and that Btk/PTK6 seems to be responsible for the Y845 phosphorylation, the retention of which confers the resistance of cancer cells to an anti-EGFR drug, cetuximab. This evidence concerns the gene EGFR and breast carcinoma.