In addition, the heterogeneity of KRAS‐mutant cancers leads to limited efficacy of KRAS inhibitors (KRASi) as monotherapy; while their combination with other targeted agents, including SHP2, EGFR, PD‐L1, CDK4/6,[10] PLK1,[11] and IRE1α,[12] significantly enhances anti‐tumor activity and overcomes resistance. Here, KRAS is linked to neoplasm.