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Endoplasmic Reticulum stress leads to protein misfolding and activation of the unfolded protein response (UPR), which promotes ROS generation, influencing cell survival and drug resistance [73]

Substrate accumulation can lead to the synthesis of other metabolic intermediates through normally inactive enzymatic reactions [3, 4]

Benefit duration remains a major concern

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Rational combinations of third-generation EGFR TKIs with anti-angiogenic drugs, chemotherapy, the EGFRMET bispecific antibody amivantamab or local tumour ablation are under investigation as strategies to delay resistance, prolong the duration of response and maximize treatment efficacy