CRC cells frequently remodel their TCA cycle due to mutations (KRAS, TP53), hypoxia, or dysregulated signaling, leading to intracellular accumulation and extracellular release of specific intermediates—including succinate, fumarate, itaconate, and α-ketoglutarate (α-KG)—which function as potent immunometabolites by directly modulating immune cell metabolism, epigenetic programming, and signaling pathways (Figure 3). Here, TP53 is linked to colorectal carcinoma.