Interestingly, the expression of markers of the ATP-ubiquitin-dependent protein degradation (e.g., ubiquitin ligases Atrogin-1 and MuRF-1 and protein ubiquitination), typically altered in cachexia [43], were only modestly affected by MKI treatments, thus suggesting that other mechanisms were likely involved in promoting skeletal muscle wasting. The gene discussed is FBXO32; the disease is Cachexia.