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In parallel, DTP cells exploit compensatory signaling circuits, including pathways such as AURKB, JNK, PI3K, and FAK-YAP, which remain active when major oncogenic drivers such as EGFR, BRAF, or MEK are inhibited ( DTP states can arise under different therapeutic exposure paradigms, including acute high-dose treatment and chronic, continuous drug exposure

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These research areas aim to meet the individualized needs of DED patients, thus paving the way for more efficient, safer, and personalized treatment approaches

The common safety discussion around this ingredient involves a manufacturing byproduct called 1,4-dioxane