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In order to continue tumor growth, oncogenes or carcinogenic signaling contribute to avoid ferroptosis and thus also allow resistance toward treatments ( In ferroptosis resistant melanoma cells, CHAC1 was shown to be upregulated by NRF2 independent from ER stress signaling alongside the Aldo-Keto Reductase Family 1 Member C1 (AKR1C1) capable of degrading lipid radicals ( CHAC1 , most melanoma cell lines appear to be resistant against ferroptosis
In support of this hypothesis, diminished expression of STIM and Orai proteins has been shown to be at the origin of decreased SOCE and increased resistance to oxidative damage in HT22 cells (Rao et al., 2013)
