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While the exact mechanism remains to be shown, the repression of JNK phosphorylation by ILK in this tumor subtype may occur through additional intermediates, including a complex of ILK-associated serine/threonine phosphatase 2C (ILKAP) with apoptosis signal–regulating kinase 1 (ASK1)
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these functions are mediated by the mitochondrial protein translocation-associated degradation (mitoTAD) pathway, mitochondrial-associated degradation (MAD) system, mitochondrial ubiquitin‒proteasome system (UPS), mitochondrial unfolded protein response (UPR mt ), and mitochondrial-derived vesicle carriers (MDVs)
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