Uniquely in SSA, the "Vitamin D Paradox" (low total levels with preserved bone health), the rarity of the <i>PNPLA3</i> genetic risk variant, and the metabolic toxicity of antiretroviral therapy (e.g., Efavirenz) create a distinct pathophysiological environment where standard definitions of deficiency may be inadequate.<h4>Conclusion</h4>Vitamin D deficiency is a plausible, modifiable driver of the MASLD-T2DM axis in Sub-Saharan Africa, potentially filling the risk void left by the absence of major genetic drivers like <i>PNPLA3</i>. This evidence concerns the gene PNPLA3 and type 2 diabetes mellitus.