On one hand, PC deletion leads to SQOR ubiquitination and degradation, thereby activating cGAS–STING and inducing metabolic reprogramming and renal fibrosis; on the other hand, early diabetic kidney disease may show SQOR upregulation as a compensatory response, which over time could aggravate hypoxic stress (as discussed in the text). This evidence concerns the gene SQOR and diabetic kidney disease.