Mechanistically, we conducted small RNA sequencing of the fusion-positive tumor followed by functional assays, demonstrating that FOXP2-CPED1 fusion led to loss of the 3′UTR of FOXP2, thus allowing escape from regulation by miR-27a and miR-27b and consequently resulting in aberrantly high expression of the truncated FOXP2 protein with full functional domains (Figure 1—figure supplement 1H–L). Here, CPED1 is linked to neoplasm.