Consistent with these observations, human myoblastsfrom IBM patients exhibited elevated levels of 1-deoxy-SA and 1-deoxy-Cer24:1 compared to myoblasts from healthy subjects (Figure 4E), which correlated with heightenedprotein aggregation.14 These results suggestthat VLC deoxy-SLs may act as potential disruptors of protein homeostasisin skeletal muscle, a phenomenon that can be potentially mitigatedthrough oral treatment with ALT-007. The gene discussed is GPT; the disease is inclusion body myositis.