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Among metabolic regulators, CD36, an important mediator of lipid uptake, has an emerging role in the lipid\u2010driven metabolic adaptation of cancer. CD36 facilitates the acquisition and use of exogenous fatty acids, enabling tumour cells to maintain bioenergetic homeostasis and growth. This metabolic rewiring supports tumour progression by establishing a complex metabolic symbiosis among heterogeneous cellular populations. CD36 has a significant role in determining the fate of various cancer\u2010associated cells including fibroblasts, adipocytes and immune cells. These tissue\u2010driven, cell type\u2010 and environment\u2010dependent lipid metabolic shifts allow the developing tumour to bypass metabolic stress and nutrient deprivation. While CD36\u2010mediated alterations act as a crucial survival promoter for the \u2018winners\u2019 (tumour cells and immunosuppressive myeloid\u2010derived suppressor cells or regulatory T\u00a0cells), they simultaneously trigger exhaustion, lipid peroxidation and ferroptosis in the \u2018losers\u2019 (cytotoxic T\u00a0cells and natural killer cells). Consequently, CD36 functions as an essential metabolic \u2018emergency exit\u2019, allowing the tumour to escape starvation and survive despite recent therapies. This review synthesises current knowledge on CD36 as a metabolic bridge linking lipid uptake, metabolic symbiosis and tumour immune ecosystem remodelling. We discuss how CD36\u2010driven lipid metabolism integrates cellular crosstalk, nutrient competition to sustain progression in different cancers. 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