SGCB and autoimmune thyroid disease: Potential molecular amplifiers include: (i) oxidative stress in the endometrium and follicular fluid (NADPH oxidase activity, mitochondrial reactive oxygen species) influences BH4 oxidation and eNOS coupling; (ii) the ADMA/DDAH equilibrium regulates substrate availability; (iii) thyroid autoimmunity and subclinical inflammation modify cytokine and redox balance, affecting nitric oxide half-life and sGC sensitivity; (iv) stimulation strategies influence granulosa cAMP and VEGF expression, indirectly affecting perfusion and, subsequently, nitric oxide diffusion kinetics [54,55].