RBM10 and TARP syndrome: The first study, using PAR-CLIP, overexpression, knockdown and RNA-Seq in HEK293 non-transformed, immortalized human embryonic kidney cells, was the first to demonstrate that RBM10 can indeed function to regulate alternative splicing, mediating preferential exon exclusion in a number of pre-mRNAs associated with TARP syndrome and cancer [3].