Since malfunctions in alternative splicing can cause many diseases, such as hypercholesterolemia, premature aging, neurodegenerative diseases, and cancer, finding small-molecule antagonists that can inhibit Hub1/Snu66 interactions could not only allow the understanding of the mode of action of Hub1 in living organisms, but it may also start new approaches to anticancer therapy in the future [2,8]. This evidence concerns the gene UBL5 and familial hypercholesterolemia.