diff --git a/modules/m66480/index.cnxml b/modules/m66480/index.cnxml
index c45759c85..d24022c71 100644
--- a/modules/m66480/index.cnxml
+++ b/modules/m66480/index.cnxml
@@ -32,7 +32,7 @@
 <section id="fs-id2853861"><title>Tumor Suppressor Genes</title><para id="fs-id1802262">Like proto-oncogenes, many of the negative cell-cycle regulatory proteins were discovered in cells that had become cancerous. <term id="term-00003">Tumor suppressor genes</term> are segments of DNA that code for negative regulator proteins, the type of regulators that, when activated, can prevent the cell from undergoing uncontrolled division. The collective function of the best-understood tumor suppressor gene proteins, Rb, p53, and p21, is to put up a roadblock to cell-cycle progression until certain events are completed. A cell that carries a mutated form of a negative regulator might not be able to halt the cell cycle if there is a problem. Tumor suppressors are similar to brakes in a vehicle: Malfunctioning brakes can contribute to a car crash!</para>
 <para id="fs-id1910594">Mutated p53 genes have been identified in more than 50 percent of all human tumor cells. This discovery is not surprising in light of the multiple roles that the p53 protein plays at the G<sub>1</sub> checkpoint. A cell with a faulty p53 may fail to detect errors present in the genomic DNA (<link target-id="fig-ch10_04_01"/>). Even if a partially functional p53 does identify the mutations, it may no longer be able to signal the necessary DNA repair enzymes. Either way, damaged DNA will remain uncorrected. At this point, a functional p53
 will deem the cell unsalvageable and trigger programmed cell death (apoptosis). The damaged version of p53 found in cancer cells, however, cannot trigger apoptosis.</para><note id="fs-id1433250" class="visual-connection">
-<para id="fs-id1984735"><figure id="fig-ch10_04_01" class="  "><media id="fs-id847150" alt="Part a: This illustration shows cell cycle regulation by normal lower case p 5 3, which arrests the cell cycle in response to D N A damage, cell cycle abnormalities, or hypoxia. Once the damage is repaired, the cell cycle restarts. If the damage cannot be repaired, apoptosis meaning programmed cell death, occurs. Part b: Mutated p 5 3 does not arrest the cell cycle in response to cellular damage. As a result, the cell cycle continues, and the cell may become cancerous.">
+<para id="fs-id1984735"><figure id="fig-ch10_04_01" class="  "><media id="fs-id847150" alt="Part a: This illustration shows cell cycle regulation by normal lower case p 5 3, which arrests the cell cycle in response to D N A damage, cell cycle abnormalities, or hypoxia. Once the damage is repaired, the cell cycle restarts. If the damage cannot be repaired, apoptosis, meaning programmed cell death, occurs. Part b: Mutated p 5 3 does not arrest the cell cycle in response to cellular damage. As a result, the cell cycle continues, and the cell may become cancerous.">
 <image mime-type="image/png" src="../../media/Figure_10_04_01-9310.png" width="500"/>
 </media>
 <caption>The role of normal p53 is to monitor DNA and the supply of oxygen (hypoxia is a condition of reduced oxygen supply). If damage is detected, p53 triggers repair mechanisms. If repairs are unsuccessful, p53 signals apoptosis. A cell with an abnormal p53 protein cannot repair damaged DNA and thus cannot signal apoptosis. Cells with abnormal p53 can become cancerous. (credit: modification of work by Thierry Soussi)</caption></figure></para>