Various CKD models, including the unilateral ureteral obstruction (UUO), I/R, FA‐induced renal fibrosis, ablation and infarction (A/I), adenine‐induced CKD, STZ‐induced and db/db DKD mouse models, as well as models of polycystic kidney disease (PKD) and hypertensive nephropathy, have consistently demonstrated that lactate accumulation activates the transcription factor hypoxia‐inducible factor 1‐alpha (HIF‐1α) and pathways such as mechanistic target of rapamycin complex 1 (mTORC1). This evidence concerns the gene HIF1A and chronic kidney disease.