This heightened oxidative state suppresses AXL receptor tyrosine kinase expression; in the same setting, AXL reduction is observed after hyperforin exposure, although the study did not test whether AXL suppression is directly caused by oxidative stress or HMOX1 [40], thereby impairing downstream AKT/ERK signaling crucial for melanoma cell invasion and metastasis. Here, HMOX1 is linked to melanoma.