Background/Objectives: SLC13A5 encodes a sodium–citrate cotransporter implicated in early‐onset epileptic encephalopathy and metabolic brain dysfunction, yet its devel-opmental regulation and molecular context in the human brain remain incompletely defined. Methods: Leveraging human developmental transcriptomes from the Evo-Devo resource, we delineated tissue trajectories and network context for SLC13A5 across the fetal–postnatal life. Results: In the cerebrum, SLC13A5 expression rises from late fetal stages to peak in the first postnatal year and then declines into adulthood, while cerebellar levels increase across the lifespan; liver shows a fetal decrease followed by sustained postnatal upregulation. A transcriptome-wide scan identified extensive positive and negative associations with SLC13A5, and a signed WGCNA built on biweight midcor-relation placed SLC13A5 in a large module. The module eigengene tracked brain mat-uration (Spearman ρ = 0.802, P = 8.62×10⁻⁶) and closely matched SLC13A5 abundance (ρ = 0.884, P = 2.73×10⁻⁶), with a significant partial association after adjusting for developmental rank (ρ = 0.672, P = 6.17×10⁻⁴). Functional enrichment converged on oxidative phos-phorylation and mitochondria. A force-directed subnetwork of the top intramodular members (|bicor| > 0.6) positioned SLC13A5 adjacent to a densely connected nucleus including CYP46A1, ITM2B, NRGN, GABRD, FBXO2, CHCHD10, CYSTM1, and MFSD4A. Conclusions: Together, these results define a developmentally tuned, mito-chondria-centered program that co-varies with SLC13A5 in the human brain across the lifespan. It may provide insights to interrogate age-dependent phenotypes and therapeutic avenues for disorders involving citrate metabolism.