We hypothesize that PM contribute to GDM pathophysiology through a cascade of events: initial interference with proteins (e.g., STAT3, AKT1, TP53) and pathways (HIF-1, thyroid hormone) drives inflammatory responses, oxidative stress, and insulin signaling defects, ultimately disrupting the balance of metabolic pathways (PPARγ, AMPK, PI3K/AKT/mTOR) and synergistically leading to insulin resistance and β-cell dysfunction (Fig 6). This evidence concerns the gene MTOR and gestational diabetes.