Together, these findings argue that both cyclin T1 and CDK9 play significant functional roles in maintaining Mcl-1 expression in bortezomib-resistant or -sensitive cells, and that the consequences of genetic disruption of the P-TEFb apparatus can be recapitulated by pharmacological CDK9 inhibitors, including in bortezomib-resistant MM cells. Here, MCL1 is linked to Miyoshi myopathy.