IF staining for α-Tubulin and DAPI revealed that chromosomal plate width increased and mitotic spindle length decreased in BTZ-treated CHEK1-OE ARP1 and H929 cells relative to both vehicle-treated CHEK1-OE cells and WT cells, suggesting that CHEK1-induced CIN was an important contributor to MM drug resistance (Fig. 3F). Here, CHEK1 is linked to Miyoshi myopathy.