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Calcium entry through the compromised plasma membrane has been shown to activate proteases (calpain, calcineurin), resulting in neurofilament degradation, disruption of axonal transport, and functional failure (Schlaepfer, 1974, 1987)

Carrying the heterozygous mutation of BRCA1/2 , transformation to complete malignancy of cells occurs after a serious external secondary hit, further resulting in genome instability and cellular disorders

In contrast, TrxR1 knockout in pancreatic cancer cells increases protection against ferroptosis via upregulated levels of GPX4 [106]

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