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If considering infectious and other non-cancer cases where alterations of oxidative and anti-oxidative therapies may be considered I personally observe the same separation of a day between each therapy type
267 GAS6, secreted by stromal cells such as CAFs and macrophages, binds to AXL, promoting its dimerization, autophosphorylation, and activation of downstream survival pathways, including the PI3K/AKT, MAPK/ERK, and NF-B pathways
The practical consequence is that identity and activity can diverge for this molecule: material could assay as present while having partially converted to a form the founding paper reported as far less active
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