As FAK inhibition is in clinical testing for Kirsten rat sarcoma virus (KRAS) oncogene-mutated non–small cell lung cancer (NSCLC; ref. 25) and low-grade serous ovarian cancer (LGSOC; ref. 26) as a therapy targeting “resistance” pathways activated by Ras/RAF/MEK pathway inhibition, our results linking FAK to the prevention of ERK activation via elevated MKP1 phosphatase expression in response to cisplatin stress may be associated with an alternate survival pathway in HGSOC. This evidence concerns the gene KRAS and non-small cell lung carcinoma.