As one of these two driver mutations are present in almost 20% of non-small cell lung cancers (NSCLC), targeting ERK signalling in combination with the use of TKI's may be a viable strategy to forestall or prevent TKI resistance and loss of DUSP6/MKP-3 is worthy of wider study as a possible ERK-mediated drug resistance mechanism in other tumour types driven by abnormal tyrosine kinase activity. The gene discussed is MAPK1; the disease is neoplasm.