The results revealed that mutations of phosphorylation sites (Y1234 and Y1235) disrupted the interaction between MET and CDKN2A in PI-resistant KAS-6/1 and U266 cells (Fig. 5D and Supplementary Figure S8C) but not affected MUC20 protein level (Supplementary Figure S10), suggesting that MUC20 should block the interaction between MET and CDKN2A by suppressing MET phosphorylation in PI-resistant MM cells. Here, MUC20 is linked to Miyoshi myopathy.