[51] However, an initial study revealed that competitive inhibition of endogenous RUNX1 function by transfection of AML1a, a naturally occurring gene product of a RUNX1 splice variant, induced cell death in most neuroblastoma cell lines, suggesting that physiological levels of RUNX1 may be essential to maintain continuous neuroblastoma cell growth [52]. The gene discussed is RUNX1; the disease is neuroblastoma.