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1 In contrast, in cancer, where malignant cells exploit heightened proteostasis resilience to tolerate genomic instability and therapeutic stress, strategically destabilizing resilience may enhance therapeutic vulnerability

Nature 523 , 183188 (2015)

During TB, IFN-I signaling-mediated recruitment of inflammatory monocytes augments the intracellular permissibility of monocytes and promotes their differentiation into an Mtb-tolerant M2 macrophage cell type with a non-inflammatory phenotype, while reducing monocyte differentiation into dendritic cells and impairing antigen presentation and T-cell priming (142)

They mean the FDA found problems during inspections