Specifically, increased PD-L1 expression appears to be driven by a number of cell-intrinsic programs—in the setting of PTEN loss in malignant brain tumors [21], activating EGFR mutations in non-small cell lung cancer [34], and increased STAT3 and AP-1 transcriptional activation in BRAF-mutant melanomas resistant to BRAF inhibition [35]. The gene discussed is EGFR; the disease is melanoma.