This is in contrast to the KMS11 and LP1 MM lines (Figure 4B, C) which have FGFR3 overexpression and constitutive activation resulting from the t(4∶14) translocation [3]–[5], as well as elevated NFκB activity due to loss of function mutations in TRAF3, which may account for the dampened ligand responsiveness [26], [27]. Here, NFKB1 is linked to Miyoshi myopathy.