Another EGFR-dependent but kinase-independent mechanism was described by Tan et al. [171], who used wide-field immunofluorescence microscopy to show that whilst the loss of EGFR expression inhibited autophagy in MDA-MB-231, HeLa, A431, and HEK293 cancer cells, re-expression of a kinase-dead mutant EGFR (K745A) rescued autophagy via EGFR’s interaction with the late endosome/lysosomal marker LAPTM4B [192] and the recruitment by the EGFR/LAPTM4B complex of the exocyst Sec5 component [193] (Figure 5C). The gene discussed is LAPTM4B; the disease is cancer.