Its overexpression drives tumour proliferation, invasion and chemoresistance via distinct molecular axes: (1) Transcriptional coactivation: BRG1 directly binds to promoters of proto‐oncogenes (e.g., ABCC3, SMAD6) [74, 75] and amplifies c‐MYC‐driven hepatocarcinogenesis, with conditional ablation in c‐MYC‐transgenic mice abolishing HCC development [76, 77]; (2) Lipid metabolic reprogramming: BRG1 suppresses glycosylated lysosomal membrane protein (GLMP) transcription, thereby inhibiting lysosomal lipid degradation and promoting lipid droplet accumulation. The gene discussed is MYC; the disease is neoplasm.