In lung and breast cancer, including EGFR-mutant NSCLC cells treated with EGFR inhibitors, drug-tolerant persisters show an increase in methylation on K116 of PRC member Jarid2, which helps stabilize and recruit PRC2 to chromatin, according to proteome-wide comparisons of lysine methylation patterns [86]. The gene discussed is EGFR; the disease is breast cancer.