Additionally, the presence of STAT family members, especially STAT3, as potential targets is interesting as STAT3 signaling has been found to be constitutively activated in RMS, and the small molecule inhibitors LLL12 and FLLL32 were reported to inhibit STAT3 activity, and inhibit the proliferation and viability of rhabdomyosarcoma cell lines more efficiently than a number of previous JAK/STAT pathway inhibitors, as well as curcumin [50]. The gene discussed is SOAT1; the disease is rhabdomyosarcoma.