Oxidative phosphorylation (p < 0.005) [21] and G2M checkpoint (p < 0.05) pathways were significantly enriched only in patients with MM, while a decrease was observed in IL6/JAK/STAT3 (p < 0.05) signaling (led mostly by negative pathway regulators such as CD38 or PTPN1 [S1 File]), in KRAS signaling (p < 0.05) (including KRAS activators, while conversely there was high KRAS expression in MM patients) and in complement (p < 0.05) pathways. Here, STAT3 is linked to Miyoshi myopathy.