Therefore, in addition to repositioning FLT3 inhibitors as a means of blocking the transcription of TAZ, we propose a new clinical indication for YAP/TAZ-TEAD PPI (protein–protein interaction) inhibitors for the treatment of CML patients that could restore TKI sensitivity and impede BP progression by blocking TAZ nuclear translocation, TAZ-TEAD interaction, and the expression of TEAD target genes such as CD36. The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.