Nerve growth factor (NGF) stimulates proliferation in glial cells through activation of the canonical Ras/Raf/MAPK pathway. However, LN229 cells, a tumour-derived glial blastoma cell line, exhibit uncontrolled proliferation even in the absence of NGF or any other growth factors. You are investigating the role of the nerve growth factor receptor (NGFR), a receptor tyrosine kinase which binds NGF, in signalling in LN229 cells. Your first hypothesis is that the dysregulation of proliferation in LN229 cells is due to increased activity of NGFR compared to a wild-type glial cell line. You discover that there is no difference in NGFR levels between the LN229 cells and a wild-type glial cell line. So now you assume the dysregulation in proliferation is due to a mutation in NGFR.

What kind of mutation could account for this difference in proliferation but not in overall receptor protein levels?