Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Q: In the mean time, Maha Nawrahta opened the southern front on 23 October 1765 in three directions. He had 20,000 to 30,000 under his command. A small army invaded by the Three Pagodas Pass towards Suphanburi. Another small army invaded down the Tenasserim coast towards Mergui and Tenasserim town. However, the main thrust of his attack was at Kanchanaburi. His 20,000-strong main southern army invaded via the Myitta Pass. Kanchanaburi fell with little resistance. The main reason for the quick fall of Kanchanaburi could be that the Burmese were more battle-hardened. But it could also be that the Siamese command miscalculated where the Burmese main attack would come from, and had not sufficiently reinforced the fort to withstand a major attack. Judging by the Siamese chronicles' reporting of the main attack route, the Siamese command appeared to have believed that the main Burmese attack would come from the Gulf of Siam coastline, instead of the most obvious and shortest route via Kanchanaburi. The Siamese sources say that Maha Nawrahta's main invasion route came from southern Tenasserim, crossing the Tenasserim range at Chumphon and Phetburi. The path is totally different from the Kanchanaburi route reported by the Burmese chronicles. Historian Kyaw Thet specifically adds that the main attack route was via the Myitta Pass.

A: How many Maha Nawrahta opened the southern front?
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Q: Anjali Lavania was born in Mumbai, Maharashtra, India.

A: What country was Anjali Lavania from?
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Q: Interleukin-6 (IL-6) can activate downstream signaling pathways in lung cancer cells, such as the STAT3 pathway, and is reported to be produced by tumor cells with activating EGFR mutations. We examined IL-6/STAT3 in lung cancer tumor tissues and the effects of siltuximab, a neutralizing antibody to human IL-6, in mouse models of lung cancer. IL-6 and STAT3 activation levels were compared with tumor histology and presence of KRAS mutations in snap-frozen, non-small-cell lung cancer tumors. The effects of siltuximab alone or in combination with erlotinib were examined in mouse xenograft models constructed using three cell line xenograft models and one primary explant mouse model. We examined the influence of cancer-associated fibroblasts (CAFs) on tumor growth and siltuximab effects. IL-6 levels were higher in tumors of squamous cell versus adenocarcinoma histology and were not associated with presence of KRAS mutations. Tyrosine phosphorylation status of STAT3 did not correlate with tumor IL-6 levels. Serine phosphorylation of STAT3 was correlated with KRAS mutation status. Both tumor and stromal cells contributed to total IL-6 within tumors. Siltuximab had minimal effect as a single agent in xenografts with tumor cells alone; however, in models coadministered with CAFs, siltuximab had more potent effects on tumor inhibition. We observed no effects of combined erlotinib and siltuximab. IL-6 is elevated in subsets of human NSCLCs, especially with squamous cell histology. Tumors supported by stromal production of IL-6 seem to be the most vulnerable to tumor growth inhibition by siltuximab.

A:
Which interleukin is blocked by Siltuximab?
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