However, multiple levels of cross-regulation between miR-223 and NOTCH1 may contribute to T-ALL, considering that NOTCH1 signaling can also repress miR-223 leading to upregulation of insulin-like growth factor-1 receptor (IGF1R), which is important for LIC activity in T-ALL [101,121]. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.