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Evasion of programmed cell death represents a critical form of oncogene addiction in cancer cells. Understanding the molecular mechanisms underpinning cancer cell survival despite the oncogenic stress could provide a molecular basis for potential therapeutic interventions. Here we explore the role of pro-survival genes in cancer cell integrity during clonal evolution in non-small cell lung cancer (NSCLC). We identify gains of  MCL-1  at high frequency in multiple independent NSCLC cohorts, occurring both clonally and subclonally. Clonal loss of functional  TP53  is significantly associated with subclonal gains of  MCL-1 . In mice, tumour progression is delayed upon pharmacologic or genetic inhibition of MCL-1. These findings reveal that  MCL-1  gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically.