Supporting this hypothesis, seborrheic keratoseslesions from a melanoma patient showed increased EGFR levels compared to control skin.21 Although increased EGF levels were not observed in ESK patients, TGF-α levelswere elevated and became undetectable after treatment, suggesting that TGF-α is themain driver of ESK.21,22 In addition, TGF-α have previously been shown to be upregulated in precursorlesions of gastric carcinomas.23 Thus, it is plausible that ESK may be correlated with EGFR mediatedproliferation of keratinocytes caused by growth factors secreted by the tumor. This evidence concerns the gene EGFR and neoplasm.