Finally, we also identified remarkable effects on effectors in cell cycle (CDKN1A) and UPR/mTOR signalling pathways (DDIT3, DDIT4, TXNIP) and the Tribble family Ser/Thr pseudokinase (TRIB3) [75] which altogether may crosstalk with glucocorticoid receptor signalling and GC therapy response in MM cells [76], [77], [78] (Fig. 9B). The gene discussed is MTOR; the disease is Miyoshi myopathy.