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The obese mice were prone to liver cancer, and their tumors showed high concentrations of molecules, called proinflammatory cytokines, that trigger inflammation.

These mice were prone to fractures and could not survive long after birth.

In addition, the fiber bundles from HOM mice, and to a lesser extent from HET mice, were prone to passive-stretch-induced fiber ruptures (Fig.  7f).

None of the R26loxpTA-p57 k /+ /Mlc2v-Cre k /+ mice were prone to early lethality over 2 years of observation suggesting that cardiac specific overexpression of p57 Kip 2 is well tolerated from the very early stages of myocardial differentiation.

PON1-knockout mice were prone to develop atherosclerotic plaques when fed a high-fat diet (Shih et al. 1998), and these animals had increased oxidative stress in both serum and macrophages (Rozenberg et al. 2003).

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It was reported that genetically-engineered RASAL2 knockout mice are prone to development of several sporadic tumor, including lung adenocarcinoma.

Conversely, the Nrf2-knockout mice are prone to acute damages and tumor formation induced by various harmful chemicals (Ramos-Gomez et al., 2001; Wang et al., 2008).

RASSF1A-knockout mice are prone to spontaneous and induced tumorigenesis [19], [20].

Therefore, while these results are not conclusive for astrogliosis, they suggest that Nrf2−/− mice are prone to MPTP-induced microgliosis.

It was recently demonstrated that Tregs in pancreatic tissue of NOD mice are prone to apoptosis because of insufficient levels of IL-2 [37].

Gfi1−/− mice are prone to inflammatory reactions characterized by increased systemic cytokine levels [17], [18] that might constitute extrinsic factors influencing B cell differentiation.

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