EGFR and familial pancreatic carcinoma: Together, these results provide an alternative and complementary mechanism to the dimerization hypothesis associated with sialyltransferase-mediated increases in sialylation and helps explain how increased flux-based sialylation attenuates EGFR signaling and holds anti-cancer potential for treating drug resistant pancreatic cancer despite resistance to TKIs or constitutive Ras activation (Figure 8 and references [69, 70]).