SMAD4 and cancer: Low throughput candidate gene sequencing studies in Capan-1 have previously identified three homozygous SNVs in KRAS, SMAD4 and MAP2K4. Using exome sequencing, we were able to detect all three of these changes: the KRAS c.35G>T mutation that causes the clinically relevant p.G12V amino acid substitution [32], [33], the c.1028C>G SNV in SMAD4 that results in a premature stop codon [34] and the MAP2K4 c.661G>T mutation in Capan-1, which leads to a cancer-associated protein truncation [35].