A heatmap summarizing genotype–MASLD associations confirmed this gradient, showing very low prevalence of steatosis (<15%) in patients with biallelic variants in LPL, APOC2, GPIHBP1, or LMF1, and markedly higher rates (>65%) among APOC3/APOB variant carriers and polygenic cases, reinforcing the ‘two-hit’ model of hepatic overproduction and systemic TG excess (Figure 3). Here, APOC3 is linked to steatosis.