Considering that hyperglycemia is known to elevate the EC risk, potentially through augmenting GLUT1 activity and facilitating passive glucose transport,[44, 45, 46] we hypothesized that normoglycemic condition (approximately 5 mmol L−1 glucose) might attenuate MGAT4A/GAL9‐driven cellular processes compared to hyperglycemic condition (approximately 20 mmol L−1 glucose). The gene discussed is MGAT4A; the disease is Hyperglycemia.