A previous study suggested that the transcriptional regulator TFII‐I interacted with the FF domains of ARHGAP35, and this interaction diminished TFII‐I transcriptional activity, owing to the cytoplasmic sequestering of TFII‐I.[24] However, in this study, the suppression of cancer cell motility by ARHGAP35 by binding to TFII‐I was unlikely because TFII‐I was almost exclusively found in the nucleus while ARHGAP35 was mainly localized in the cytoplasm. Here, GTF2I is linked to cancer.