Taken together, our research described four important findings (Figure 5): (1) That knockdown of TβRII could inhibit the proliferation of mK3 cells; (2) that the expression of Six2 was inhibited after the knockdown of TβRII; (3) that TβRII regulated the proliferation of MM cells through Six2; (4) that the activation of the TGFβ signaling pathway increased the expression of Six2; (5) that TβRII regulated Six2 through the transcriptional regulation of Smad3. The gene discussed is TGFBR2; the disease is Miyoshi myopathy.