Pancreatic cancer, with its rapidly evolving tumor genomes, oncogenic K-RAS signaling plasticity and network adaptability, and immense tumor/TME heterogeneity, can easily bypass, rewire, and re-activate its formidable K-RAS signaling network via numerous possible combinations of synergistic compensatory RAS effector pathway activation to re-stimulate tumor growth. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.