As diabetic animal studies previously reported that SGLT2i attenuates both systemic and renal tissue inflammation [23], the latter being a prominent mediator of diabetic and non-diabetic CKD [24], we aimed at elucidating the pathways involved in SGLT2i-mediated nephroprotection by using a systematic molecular approach in two independent HPTC lines, utilizing IL-1β as a pro-inflammatory mediator. This evidence concerns the gene IL1B and chronic kidney disease.