Specifically, they identified IL-6 as a direct target of ARID1A tumor-suppressor activity and suggested that under the absence of the negative regulation of the latter, coexisting amplification of PIK3CA promoted IL-6 overexpression, thus maintaining the JAK/STAT signaling loop [101], which in turn positively interconnects with the mTOR pathway [102,103,104]. The gene discussed is SOAT1; the disease is neoplasm.