text_1: B3-Galectin decreases cell resistance to tyrosine kinase inhibitors (TKIs) by engaging the alternate KRAS-RalB signaling complex downstream of EGFR.
text_2: Mechanistically, αvβ3, in the unliganded state, recruits KRAS and RalB to the tumour cell plasma membrane, leading to the activation of TBK1 and NF-κB. In fact, αvβ3 expression and the resulting KRAS–RalB–NF-κB pathway were both necessary and sufficient for tumour initiation, anchorage independence, self-renewal and erlotinib resistance.