The study investigates the role of tubular CPT1A in aging and chronic kidney injury. Mice with tubule-specific deletion of Cpt1a (Cpt1a^flx/ flx) were aged for 2 years or subjected to aristolochic acid nephropathy (AAN) or unilateral ureteral obstruction (UUO). Surprisingly, these mice showed no significant differences in kidney function or fibrosis compared to wild-type mice. Primary tubule cells from aged Cpt1a^flx/ flx mice had a modest decrease in palmitate oxidation but retained the ability to metabolize long-chain fatty acids. Very-long-chain fatty acids, which are exclusively oxidized by peroxisomes, were reduced in kidneys lacking tubular CPT1A, suggesting increased peroxisomal activity. Single-nucleus RNA-Seq revealed significantly increased expression of peroxisomal FAO enzymes in proximal tubules of Cpt1a^flx/ flx mice. These findings suggest that peroxisomal FAO may compensate for the absence of CPT1A, and further genetic studies are needed to confirm this role.The study investigates the role of tubular CPT1A in aging and chronic kidney injury. Mice with tubule-specific deletion of Cpt1a (Cpt1a^flx/ flx) were aged for 2 years or subjected to aristolochic acid nephropathy (AAN) or unilateral ureteral obstruction (UUO). Surprisingly, these mice showed no significant differences in kidney function or fibrosis compared to wild-type mice. Primary tubule cells from aged Cpt1a^flx/ flx mice had a modest decrease in palmitate oxidation but retained the ability to metabolize long-chain fatty acids. Very-long-chain fatty acids, which are exclusively oxidized by peroxisomes, were reduced in kidneys lacking tubular CPT1A, suggesting increased peroxisomal activity. Single-nucleus RNA-Seq revealed significantly increased expression of peroxisomal FAO enzymes in proximal tubules of Cpt1a^flx/ flx mice. These findings suggest that peroxisomal FAO may compensate for the absence of CPT1A, and further genetic studies are needed to confirm this role.