KRAS and cancer: In contrast, Endoplasmic Reticulum (ER) stress, which has been identified as a therapeutic target in KRAS mutant cancers25 caused a significant increase in the ER marker HSPA5 (also known as GRP78) and in KRAS4B, but not KRAS4A, in both A549 and SUIT2 cancer cell lines (Fig. 5D, E).