In fact, TLR-4 was identified as the receptor for LPS by positional cloning of its gene from the LPS-resistant C3H/HeJ mouse strain, which harbors a naturally occurring mutation in the cytoplasmic tail of TLR-4 that interferes with the receptor’s ability to signal. When we discuss septic shock more fully later in the chater, we shall see that it is an undesirable consequence of the same effector actions of TNF-α that are important in containing local infections.