Evidence is presented indicating that IR is a strong mediator of YB-1 phosphorylation only in tumor cells with wild-type K-RAS (K-RASwt); in tumor cells with mutated K-RAS (K-RASmut), YB-1 is constitutively phosphorylated, and this phosphorylation cannot be further enhanced by exposure to IR. This evidence concerns the gene KRAS and neoplasm.