Drugging MEK as a downstream target of activated MAPK signaling might therefore be a promising therapeutic approach for the treatment of vemurafenib-resistant tumours [20, 39, 40]; the results presented here suggest a possible additional use of MEK inhibition through the impairment of DDR and enhanced apoptosis, possibly via downregulation of hnRNP K. This evidence concerns the gene HNRNPK and neoplasm.