CLK2 and neoplasm: The AS of TGFBR2 occurred at the non-canonical splice sites and resulted in a selective exclusion of TGFBR2 mRNA sequences that code for TGFBR2 regions involved in tumor suppressive interactions such as ATM, CLK2, and CDC2, whereas the TGFBR2 sites related to the tumor promoting interactions such as interactions with MAPK1, PDK1, and PRKCZ were maintained in these aberrant transcripts (Sivadas et al., 2014).