This suggests 3 potential explanations: the observed T2D–EC association may be mediated through pathways independent of chronic hyperglycemia, such as insulin signaling or chronic inflammation; the glycemic control threshold required for cancer risk modulation may exceed the physiological range captured by common HbA1c-associated SNPs; or the limited statistical power due to the modest case number (n = 232) in the FinnGen EC GWAS may have constrained our ability to detect a true effect. This evidence concerns the gene INS and cancer.