Broadly, the proposed mechanisms include1 initial resistance, which limits chemotherapeutic agent accumulation inside cells2; direct resistance, facilitated by DNA repair proteins like ERCC1 and systems such as homologous recombination (e.g., BRCA)3; subsequent resistance, involving alterations in apoptosis pathways (e.g., changes in p53, BCL‐2)4; indirect resistance, which occurs via pathways not directly affected by cisplatin, such as ERBB2/EGFR; and5 disruptions in tumour angiogenesis reducing chemotherapeutic delivery.20 The gene discussed is BCL2; the disease is neoplasm.