EHMT2 overexpression was observed in erlotinib resistance in NSCLC, leading to transcriptional activation of PTEN and repressed Akt signaling, whereas inhibition of EHMT2 reverses the acquired indifference to therapy and re-sensitizes NSCLC cells to EGFR-TKI treatment.107 Histone modifications, either via EHMT2 or histone deacetylase 3 (HDAC3), can result in acquired resistance against mitogen-activated extracellular signal-regulated kinase inhibitors (MEKi) treatment in pancreatic ductal adenocarcinoma (PDAC).108. The gene discussed is HDAC3; the disease is pancreatic ductal adenocarcinoma.