In a series of experiments, genes that code for mutant forms of an RTK are introduced into cells. The cells also express their own normal form of the receptor from their normal gene, although the mutant genes are constructed so that the mutant RTK is expressed at a considerably higher concentration than the normal RTK. What would be the consequences of introducing a mutant gene that codes for an RTK (A) lacking its extracellular domain, or (B) lacking its intracellular domain?