To determine whether the cytotoxic effects of the pharmacological inhibition of SEDT8 mediated by UNC-0379 were also dependent on p53 activation in MM cells, we compared the UNC-0379 response in p53 wild-type HMCLs (n = 7) and p53-deficient HMCLs (n = 5) [28, 41] that displayed similar SETD8 expression levels (Additional files 2 and 3: figure S8A). Here, KMT5A is linked to Miyoshi myopathy.