It has been observed that HNK inhibited MM cell growth, down-regulated Sp1 expression and Sp1 target transcription factors, including cyclin D1, Mcl-1, and survivin, and induced the apoptosis by increasing Bax, reducing Bid and Bcl-xL and activating caspase-3 and PARP [155]. The gene discussed is SP1; the disease is Miyoshi myopathy.