Interestingly, the transport of proteins through GA cisternae (vesicular vs non-vesicular including tubules) promotes distinct glycosylation pathways, and mis-glycosylation of ECM components has been implicated in tumor promoting inflammation and immunosuppression, potentially disclosing another layer of complexity in the effect of mut-p53 on the crosstalk between cancer cells and TME. The gene discussed is TP53; the disease is cancer.