While this effect of reduced LAL activity would be consistent with the pro-atherogenic effect of LAL deficiency in CESD, potential weaknesses of this study are that rs1051338 is not yet proven as the causal variant at the LIPA GWAS locus, the small sample size, and that other aspects of LAL activity such as CE hydrolysis and autophagy were not examined (Zhang and Reilly, 2017). The gene discussed is LIPA; the disease is hyperinsulinemic hypoglycemia, familial, 4.