KMT5A and Miyoshi myopathy: Since the appearance of nucleolar stress or DNA damage is sufficient to activate p53 functions [54, 55] and occurs independently of p53 upon UNC-0379 (Figs. 4 and 5), we propose that the activation of p53 upon SETD8 inhibition is mainly caused by these stress signals rather than the potential loss of SETD8-induced p53 methylation in MM cells.