In this context, it is important to underline that recent findings have highlighted how self-renewal of T-ALL LICs is driven and maintained by β-catenin via a spleen focus-forming virus proviral integration oncogene 1 (SPI1)/hepatitis A virus cellular receptor 2 (HAVCR2) regulatory circuit [48] (see later on in this article). The gene discussed is SPI1; the disease is acute lymphoblastic leukemia.