Lower levels of N-acetylneuraminate in tumors from SPI-fed rats would implicate altered cell surface glycans that are critical for pathways in cancer, including immune evasion, resistance to apoptosis, and enhanced proliferation, metastasis and angiogenesis.50–52 Notably, altered sialyation has been linked to activation of the inflammasome mediator eIF2,50 which in an APC-deficient background attenuates MYC-dependent apoptosis,53 unless circumvented by mechanisms that downregulate EIF2 – as observed for Eif2b2 in colon tumors from SPI-fed rats (Supplemental Figure S3b, green arrow). Here, APC is linked to colonic neoplasm.