2022). By using small inhibitory RNA methods to systematically knock down gene expression in cultured hepatocytes, a number of important proteins involved in controlling LDLR expression were identified. Of these, 15 were involved in the function of the U2‐spliceosome, identifying this complex and its cognate genes as potential novel FH‐causing genes. In support of this, SNPs of the RBM25 gene show a significant association with LDL‐cholesterol in several different population studies, and three rare variants were identified in individuals with FH. Here, LDLR is linked to familial hyperaldosteronism.