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This suggests that reducing FA uptake can reduce FA oxidation and lipotoxicity, improving cardiac function.90 Alternative approaches, such as reducing mitochondrial FA uptake or FA oxidation, via CPT1 inhibitors and oxidation enzyme inhibitors, respectively, show similar outcomes on metabolism.91 However, reports have suggested that long-term inhibition of CPT1 may mediate deleterious effects on myocardial lipid storage, suggesting that further characterisation may be necessary.92 Furthermore, data has indicated that the anti-anginal drug ranolazine may rebalance metabolism in T2D,93 with trials showing improvements in cardiac function in a diabetic sub-group, highlighting the potential for the repurposing of this drug.94 3