These pathways include the downstream effector protein kinase Cι (PKCι) involved in tumor-initiating cell phenotype through the PKCι/ELF3/NOTCH3 axis [21]; the EphA2 a receptor tyrosine kinase (RTK) that negatively regulates the KRAS/MEK/ERK pathway after the binding of its ligand ephrin A1 [22]; or the CUB domain–containing protein 1 (CDCP1) and AXL that are two RTKs regulated by many KRAS effectors, like RAF/MEK/ERK and PI3K/AKT/mTOR [23, 24]. The gene discussed is KRAS; the disease is neoplasm.