Hence, abnormal activation of type I IFN response in the infiltrate could misdirect the immune response and further aggravate the defective expression of antimicrobial peptides due to EGFR inhibition in keratinocytes [8], leading to high susceptibility to Staph. aureus skin infections in patients undergoing treatment with these EGFR inhibitors [8, 58]. The gene discussed is EGFR; the disease is skin infection.