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In particular, they pointed out that although NRF2 has been traditionally considered as a tumor suppressor because of its cytoprotective functions [320], a growing number of studies have shown a strong NRF2 activation at certain stages of cancer [318, 321]

Additionally, DSIP appears to be regulated by glucocorticoids, and its signaling may interact with the MAPK cascade through homology with glucocorticoid-induced leucine zipper (GILZ), suggesting potential roles in cellular stress responses

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This was highly likely due to the bacterial cells transitioning into their L-forms [78]

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