KHDRBS1 and cancer: Thus, our study reveals a new regulatory mechanism of Sam68 function, which adds to the various post-translational modifications, such as tyrosine phosphorylation (43) and acetylation (65), and interactions with regulatory partners, such as the transcriptional cofactors SND1 (54) and FBI-1 (66), that modulate its splicing activity in cancer cells, including TNBC cells.