In line with these results, a recent study performed on human MM cells demonstrates that valproic acid (VPA), a molecule originally described as an antiepileptic and then demonstrated to inhibit HDACs inducing antineoplastic activity), is able to enhance the expression of the NKG2D ligands MICA/B and ULBP-2 with a mechanism dependent on the activation of constitutively phosphorylated ERK [23]. This evidence concerns the gene KLRK1 and Miyoshi myopathy.