For example, mutations in receptor tyrosine kinase pathways, such as epidermal growth factor receptor (EGFR), have been shown to induce PD-L1 expression in lung tumors [12] and this overexpression in cancer cells can block anti-tumor immunity, resulting in immune escape [13], which can be overcome by PD-1/PD-L1 inhibition by restoring tumor-specific T-cell immunity. The gene discussed is EGFR; the disease is neoplasm.