The explanation for this observation is likely multifactorial: (i) a higher proportion of intercurrent illness in SGLT2i DKA, (ii) demographic differences with the SGLT2i group consisting of largely patients with T2D with baseline insulin resistance than the non-SGLT2i group, (iii) delayed drug clearance with the half-life of SGLT2i being approximately 12 h, and (iv) pancreatic alpha cell secretion of glucagon and consequent hyperglucagonemia from SGLT2i [21], requiring treatment with greater insulin for ketone clearance compared to non-SGLT2i DKA. This evidence concerns the gene INS and Insulin resistance.